Immunity In Early Life Research Articles

Immunity in the Very Young: Challenges and Opportunities

Immunity in early life encompasses the delicate interphase at the maternal-fetal stage, as well as rapid development and adaptation that occur as the newborn transitions from the protected maternal environment to functioning in the outside world. Understanding the forces that shape immunity in the very young and that lay the groundwork for an effective adult immune system holds both questions and promise.

The crosstalk between developing sympathetic nerves and immune cells contributes to early-life Th2 bias in the lung

Abstract The adaptive immunity in early life is polarized towards Th2 response, which contributes to increased susceptibility to asthma in children. However, the molecular mechanism of age-related Th2 bias remains poorly understood. Building upon critical roles of nerves in the modulation of immune responses, we investigated the crosstalk between the developing nervous system and the immune cells in postnatal lungs using murine models and human lung tissues/cells. Notably, like human, mice exhibit similar early-life Th2 bias, as allergen exposure elicits more robust inflammation in neonates than in adult mice. In addition, our previous studies revealed a similar profile of neurogenic factors between mouse and human lungs. Therefore, the neonatal mouse model of asthma provides an invaluable tool to identify potential modulatory roles of nerves in early life Th2 immunity bias. In this study, we identified dopamine as a potent inducer of Th2 phenotypes in a screen for the role of neurotransmitters in the differentiation of CD4+ T cells, which is consistent with a previous finding. Dopamine is selectively expressed by the sympathetic nerves in developing lungs. Besides, we discovered that sympathetic nerves transited from dopamine-producing in early life to norepinephrine-producing in adult life. We proved that the dopamine-rich sympathetic nerve played a role in allergic Th2 inflammation in neonatal mice lungs. However, with age, the level of dopamine decreased and therefore, this immune modulation reduced. Taken together, our findings reveal the crosstalk between the developing nerves and Th2 prone immunity in early life. Our study may provide the foundation for potential therapy strategies for kids with asthma.

Age-specific TLR7/8 adjuvant formulation overcomes hyporesponsiveness to neonatal acellular pertussis vaccination in a mouse model

Abstract Infection is the most common cause of mortality early in life, in large measure due to suboptimal early life vaccination strategies as compared to older age groups. New adjuvants are absolutely cardinal to further optimize current immunization approaches. However, only a few classes of adjuvants are presently incorporated in vaccines approved for human use. Recent advances in the discovery and delivery of Toll-like receptor (TLR) adjuvants have provided a new toolbox for vaccinologists. Prominent among these candidate adjuvants are synthetic small molecule TLR7/8 agonists. The development of an effective infant Bordetella pertussis vaccine is now urgent because of the resurgence of pertussis in many countries, contemporaneous and likely related to the switch from whole cell to acellular vaccines. In this context, age-specific adjuvant strategies may be key to enhance early life immunogenicity by creating a vaccine formulation that induces both robust and persistent immunity (i.e., overcome waning immunity) to B. pertussis. In the present study, we firstly optimized the a) formulation delivery system, b) stability, and c) immunologic activity of novel small molecule imidazoquinoline TLR7/8 adjuvants towards human infant leukocytes. Next, in both adult and neonatal mouse models, we demonstrate that this TLR7/8 adjuvant can overcome neonatal hyporesponsiveness to acellular pertussis vaccination by driving Th1 favoring responses to a licensed acellular vaccine (DTaP). This potent immunization strategy may be of fundamental importance in vaccine development and could represent a new paradigm for effective pertussis immunization in early life.

Leptin and adiponectin supplementation modifies mesenteric lymph node lymphocyte composition and functionality in suckling rats.

At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ + cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ + CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

Lifelong Maintenance of Oral Tolerance and Immunity Profiles in Mice Depends on Early Exposure to Antigen.

Oral tolerance is defined as a state of systemic hyporesponsiveness to an antigen that has been previously administered by the oral route. Many factors affect oral tolerance induction; some of them related to antigen, and some related to the animal. The age of the animal is one of the most important factors that affect oral tolerance as ageing brings many alterations in immune responses. Herein, we demonstrated that both the oral tolerance and pattern of immune reactivity triggered in early life were kept up to 15 months regarding the magnitude of antibody production, cell proliferation and cytokine profile when compared to immune responses induced in old mice. Therefore, our results corroborate with a promising proposal for prevaccination during childhood and young age, and a booster in older age, to make sure that the primary immunization in early life is not lost in aged individuals.

The Impact of IgG transplacental transfer on early life immunity.

Pediatric vaccines have significantly reduced infectious disease-related infant mortality, but as protective immunity often require several infant vaccine doses; maternally-acquired antibodies are critical to protect infants during the first months of life. Consequently, immunization of pregnant women is an important strategy not only to protect mothers from infection, but also to provide immunity to young infants. Nevertheless, maternal immunization can also negatively impact early life immunity. In fact, maternal antibodies can interfere with the development of infant immune responses, though it is unclear if such interference is clinically significant. Moreover, the transplacental transfer of maternal immunoglobulin therapeutics can be harmful to the fetus. Thus, the risk/benefit of maternal immunization for both the mother and the fetus should be carefully weighed. In addition, it is critical to fully understand the mechanisms by which IgG is transferred across the placenta in order to develop optimal maternal and infant immunization strategies.

The influence of developmental timing on B cell diversity.

The adult adaptive immune system is comprised of a wide spectrum of lymphocyte subsets with distinct antigen receptor repertoire profiles, effector functions, turnover times and anatomical locations, acting in concert to provide optimal host protection and self-regulation. While some lymphocyte populations are replenished by bone marrow hematopoietic stem cells (HSCs) through adulthood, others emerge during a limited window of time during fetal and postnatal life and sustain through self-replenishment. Despite fundamental implications in immune regeneration, early life immunity and leukemogenesis, the impact of developmental timing on lymphocyte output remains an under explored frontier in immunology. In this review, we spotlight recent insights into the developmental changes in B cell output in mice and explore how several age specific cellular and molecular factors may shape the formation of a diverse adaptive immune system.

γδ T Cells Contribute to Injury in the Developing Brain

Brain injury in premature infants, especially periventricular leukomalacia, is an important cause of neurologic disabilities. Inflammation contributes to perinatal brain injury development, but the essential mediators that lead to early-life brain injury remain largely unknown. Neonates have reduced capacity for mounting conventional αβT-cell responses. However, γδT cells are already functionally competent during early development and are important in early-life immunity. We investigated the potential contribution of γδT cells to preterm brain injury using postmortem brains from human preterm infants with periventricular leukomalacia and two animal models of preterm brain injury—the hypoxic-ischemic mouse model and a fetal sheep asphyxia model. Large numbers of γδT cells were observed in the brains of mice, sheep, and postmortem preterm infants after injury, and depletion of γδT cells provided protection in the mouse model. The common γδT-cell–associated cytokines interferon-γ and IL-17A were not detectable in the brain. Although there were increased mRNA levels of Il17f and Il22 in the mouse brains after injury, neither IL-17F nor IL-22 cytokines contributed to preterm brain injury. These findings highlight unique features of injury in the developing brain, where, unlike injury in the mature brain, γδT cells function as initiators of injury independently of common γδT-cell–associated cytokines. This finding will help to identify therapeutic targets for preventing or treating preterm infants with brain injury.

Identification and Characterization of Stimulator of Interferon Genes As a Robust Adjuvant Target for Early Life Immunization.

Immunization is key to preventing infectious diseases, a leading cause of death early in life. However, due to age-specific immunity, vaccines often demonstrate reduced efficacy in newborns and young infants as compared to adults. Here, we combined in vitro and in vivo approaches to identify adjuvant candidates for early life immunization. We employed newborn and adult bone marrow-derived dendritic cells (BMDCs) to perform a screening of pattern recognition receptor agonists and found that the stimulator of interferon genes ligand 2′3′-cGAMP (hereafter cGAMP) induces a comparable expression of surface maturation markers in newborn and adult BMDCs. Then, we utilized the trivalent recombinant hemagglutinin (rHA) influenza vaccine, Flublok, as a model antigen to investigate the role of cGAMP in adult and early life immunization. cGAMP adjuvantation alone could increase rHA-specific antibody titers in adult but not newborn mice. Remarkably, as compared to alum or cGAMP alone, immunization with cGAMP formulated with alum (Alhydrogel) enhanced newborn rHA-specific IgG2a/c titers ~400-fold, an antibody subclass associated with the development of IFNγ-driven type 1 immunity in vivo and endowed with higher effector functions, by 42 days of life. Highlighting the amenability for successful vaccine formulation and delivery, we next confirmed that cGAMP adsorbs onto alum in vitro. Accordingly, immunization early in life with (cGAMP+alum) promoted IFNγ production by CD4+ T cells and increased the proportions and absolute numbers of CD4+ CXCR5+ PD-1+ T follicular helper and germinal center (GC) GL-7+ CD138+ B cells, suggesting an enhancement of the GC reaction. Adjuvantation effects were apparently specific for IgG2a/c isotype switching without effect on antibody affinity maturation, as there was no effect on rHA-specific IgG avidity. Overall, our studies suggest that cGAMP when formulated with alum may represent an effective adjuvantation system to foster humoral and cellular aspects of type 1 immunity for early life immunization.

Immunization practices in low birth weight infants from rural Haryana, India: Findings from secondary data analysis.

BackgroundLow birth weight (LBW) infants constitute a vulnerable subset of infants with impaired immunity in early life. In India, there is scarcity of studies that focus on immunization practices in such infants. This analysis aimed to examine immunization practices in LBW infants with the intention to identify areas requiring intervention.MethodsData on immunization status of LBW infants enrolled in an individually randomized, double–masked, placebo–controlled trial of neonatal vitamin A supplementation were analysed. Study outcomes were full immunization by one year of age and delayed vaccination with DPT1 and DPT3. Multivariable logistic regression was performed to identify factors associated with the outcome(s).FindingsOut of 10 644 LBW infants enrolled in trial, immunization data were available for 10 517 (98.8%). Less than one–third (29.7%) were fully immunized by one year of age. Lowest wealth quintile (adjusted odds ratio (AOR) 0.39, 95% confidence interval (CI) 0.32–0.47), Muslim religion (AOR 0.41, 95% CI 0.35–0.48) and age of mother <20 years (AOR 0.62, 95% CI 0.52–0.73) were associated with decreased odds of full immunization. Proportion of infants with delayed vaccination for DPT1 and DPT3 were 52% and 81% respectively. Lowest wealth quintiles (AOR 1.51, 95% CI 1.25–1.82), Muslim religion (AOR 1.41, 95% CI 1.21–1.65), mother aged <20 years (AOR 1.31, 95% CI 1.11–1.53) and birth weight <2000 g (AOR 1.20, 95% CI 1.03–1.40) were associated with higher odds of delayed vaccination for DPT–1. Maternal education (≥12 years of schooling) was associated with high odds of full immunization (AOR 2.39, 95% CI 1.97–2.91) and low odds of delayed vaccination for both DPT–1 (AOR 0.59, 95% CI 0.49–0.73) and DPT–3 (AOR 0.57, 95% CI 0.43–0.76)ConclusionIn this population, LBW infants are at a risk of delayed and incomplete immunization and therefore need attention. The risks are even higher in identified subgroups that should specifically be targeted

Innate Immunity to Respiratory Infection in Early Life.

Early life is a period of particular susceptibility to respiratory infections and symptoms are frequently more severe in infants than in adults. The neonatal immune system is generally held to be deficient in most compartments; responses to innate stimuli are weak, antigen-presenting cells have poor immunostimulatory activity and adaptive lymphocyte responses are limited, leading to poor immune memory and ineffective vaccine responses. For mucosal surfaces such as the lung, which is continuously exposed to airborne antigen and to potential pathogenic invasion, the ability to discriminate between harmless and potentially dangerous antigens is essential, to prevent inflammation that could lead to loss of gaseous exchange and damage to the developing lung tissue. We have only recently begun to define the differences in respiratory immunity in early life and its environmental and developmental influences. The innate immune system may be of relatively greater importance than the adaptive immune system in the neonatal and infant period than later in life, as it does not require specific antigenic experience. A better understanding of what constitutes protective innate immunity in the respiratory tract in this age group and the factors that influence its development should allow us to predict why certain infants are vulnerable to severe respiratory infections, design treatments to accelerate the development of protective immunity, and design age specific adjuvants to better boost immunity to infection in the lung.

Transfer of maternal immunity and programming of the newborn immune system.

As placental mammals, the pregnant women and the fetus have intense and prolonged interactions during gestation. There is increasing evidence that multiple molecular as well as cellular components originating in pregnant women are transferred to the fetus. The transfer of maternal antibodies has long been recognized as a central component of newborn immunity against pathogens. More recent studies indicate that inflammatory mediators, micronutrients, microbial products and maternal cells are transferred in utero and influence the fetal immune system. Together, these multiple signals are likely to form a complex network of interactions that program the neonatal immune system and tune its homeostatic regulation. Maternal disorders, in particular infectious diseases, modify these signals and may thereby alter immunity in early life. Understanding maternal programming of the newborn immune system could provide a basis for interventions promoting child health.

Development of allergic immunity in early life.

The growth and maturity of the peripheral immune system and subsequent development of pulmonary immunity in early life is dictated by host, environmental and microbial factors. Dysregulation during the critical window of immune development in the postnatal years results in disease which impacts on lifelong lung health. Asthma is a common disease in childhood and is often preceded by wheezing illnesses during the preschool years. However, the mechanisms underlying development of wheeze and how and why only some children progress to asthma is unknown. Human studies to date have generally focused on peripheral immune development, with little assessment of local tissue pathology in young children. Moreover, mechanisms underlying the interactions between inflammation and tissue repair at mucosal surfaces in early life remain unknown. Disappointingly, mechanistic studies in mice have predominantly used adult models. This review will consider the aspects of the neonatal immune system which might contribute to the development of early life wheezing disorders and asthma, and discuss the external environmental factors which may influence this process.

Distinct innate signaling and activation of dendritic cells during the neonatal period determines their functional response to respiratory syncytial virus infection

Abstract Dendritic cells (DCs) are among the first to respond to infection, providing the critical link between innate and adaptive immunity. Neonates often have weak innate immune responses that can limit adaptive immunity and contribute to increased susceptibility and more severe infection with intracellular pathogens, such as respiratory syncytial virus (RSV). We have previously shown differential migration and defective activation of neonatal murine respiratory CD103+ DCs, which is associated with diminished RSV-specific CD8 T cell responses in neonatal mice. In order to define the age-dependent regulation of respiratory DC function, we have developed a neonatal mouse model of RSV to track antigen presentation via infection with an ovalbumin-expressing RSV and an antibody against H2kb-OVA257–264. We found adequate transfer of RSV-derived OVA257–264 by neonatal CD103+ DCs to the dLN, suggesting poor CD8 T cell responses are not due to limited antigen presentation. However, neonatal CD103+ DCs expressing H2kb-OVA257–264 failed to upregulate CD80/86, which is critical to T cell stimulation. RNA-seq analysis of H2kb-OVA257–264+ CD103+ DCs implicated defective type I IFN signaling in neonates that may influence reduced activation. In support of this, while we find type I IFN to be diminished in the neonatal lung, treatment of neonates with IFN-α failed to restore the activation of neonatal H2kb-OVA257–264+ CD103+DCs. Our data demonstrate a distinct developmental regulation of innate immunity in early life and identify type I IFN signaling as contributing to defective DC activation during RSV infection in neonates. Defining age-dependent mechanisms controlling immunity may lead to intelligently designed vaccines for this age group.

Neonatal MDSCs compromise macrophage control of encapsulated bacteria

Abstract Limitations in innate and adaptive immunity have been described early in life that contribute to susceptibility to microbial infection. Interleukin (IL)-27 is a heterodimeric cytokine produced primarily by antigen presenting cells and suppressive toward a variety of immune cell types. We have shown in humans and mice that neonatal macrophages express IL-27 at an elevated level as compared with adults. In mice this was shown to be maintained through infancy. Using the mouse as a model system, we have recently shown that myeloid-derived suppressor cells (MDSCs) are more abundant in the spleens of neonatal and infant mice and contribute to elevated IL-27 levels in young mice. Functional studies demonstrate that these MDSCs express active nitric oxide synthase, phagocytic oxidase complex, and arginase-1. Few studies have investigated the influence of MDSCs on innate immune function during bacterial infection. Streptococcus agalactiae and Escherichia coli are significant concerns for newborns as common causes of sepsis. We investigated the influence of neonatal and infant MDSCs cultured with infected macrophages and show impaired macrophage control of S. agalactiae and E. coli. Furthermore, the suppressive effect of MDSCs on macrophage function requires IL-27. Inclusion of a soluble receptor to neutralize IL-27 promotes increased control of bacterial growth. Our data suggests that the effect of MDSCs and IL-27 involves a direct influence on macrophage effector functions since inflammatory cytokines such as TNF and IL-6 are not significantly altered by the presence of MDSCs. Taken together these results suggest that the increased abundance of MDSCs and IL-27 production may contribute to some of the limitations in early life immunity.

Toll-like receptor 8 agonist nanoparticles mimic immunomodulating effects of the live BCG vaccine and enhance neonatal innate and adaptive immune responses

BackgroundNewborns display distinct immune responses, leaving them vulnerable to infections and impairing immunization. Targeting newborn dendritic cells (DCs), which integrate vaccine signals into adaptive immune responses, might enable development of age-specific vaccine formulations to overcome suboptimal immunization.ObjectiveSmall-molecule imidazoquinoline Toll-like receptor (TLR) 8 agonists robustly activate newborn DCs but can result in reactogenicity when delivered in soluble form. We used rational engineering and age- and species-specific modeling to construct and characterize polymer nanocarriers encapsulating a TLR8 agonist, allowing direct intracellular release after selective uptake by DCs.MethodsChemically similar but morphologically distinct nanocarriers comprised of amphiphilic block copolymers were engineered for targeted uptake by murine DCs in vivo, and a range of TLR8 agonist–encapsulating polymersome formulations were then synthesized. Novel 96-well in vitro assays using neonatal human monocyte-derived DCs and humanized TLR8 mouse bone marrow–derived DCs enabled benchmarking of the TLR8 agonist–encapsulating polymersome formulations against conventional adjuvants and licensed vaccines, including live attenuated BCG vaccine. Immunogenicity of the TLR8 agonist adjuvanted antigen 85B (Ag85B)/peptide 25–loaded BCG-mimicking nanoparticle formulation was evaluated in vivo by using humanized TLR8 neonatal mice.ResultsAlthough alum-adjuvanted vaccines induced modest costimulatory molecule expression, limited TH-polarizing cytokine production, and significant cell death, BCG induced a robust adult-like maturation profile of neonatal DCs. Remarkably, TLR8 agonist polymersomes induced not only newborn DC maturation profiles similar to those induced by BCG but also stronger IL-12p70 production. On subcutaneous injection to neonatal mice, the TLR8 agonist–adjuvanted Ag85B peptide 25 formulation was comparable with BCG in inducing Ag85B-specific CD4+ T-cell numbers.ConclusionTLR8 agonist–encapsulating polymersomes hold substantial potential for early-life immunization against intracellular pathogens. Overall, our study represents a novel approach for rational design of early-life vaccines.

Preclinical Immunomodulation by the Probiotic Bifidobacterium breve M-16V in Early Life.

This study aimed to investigate the effect of supplementation with the probiotic Bifidobacterium breve M-16V on the maturation of the intestinal and circulating immune system during suckling. In order to achieve this purpose, neonatal Lewis rats were supplemented with the probiotic strain from the 6th to the 18th day of life. The animals were weighed during the study, and faecal samples were obtained and evaluated daily. On day 19, rats were euthanized and intestinal wash samples, mesenteric lymph node (MLN) cells, splenocytes and intraepithelial lymphocytes (IEL) were obtained. The probiotic supplementation in early life did not modify the growth curve and did not enhance the systemic immune maturation. However, it increased the proportion of cells bearing TLR4 in the MLN and IEL, and enhanced the percentage of the integrin αEβ7+ and CD62L+ cells in the MLN and that of the integrin αEβ7+ cells in the IEL, suggesting an enhancement of the homing process of naïve T lymphocytes to the MLN, and the retention of activated lymphocytes in the intraepithelial compartment. Interestingly, B. breve M-16V enhanced the intestinal IgA synthesis. In conclusion, supplementation with the probiotic strain B. breve M-16V during suckling improves the development of mucosal immunity in early life.

Distinct TLR-mediated cytokine production and immunoglobulin secretion in human newborn naïve B cells.

Neonatal innate immunity is distinct from that of adults, which may contribute to increased susceptibility to infection and limit vaccine responses. B cells play critical roles in protection from infection and detect PAMPs via TLRs, that, when co-activated with CD40, can drive B-cell proliferation and Ab production. We characterized the expression of TLRs in circulating B cells from newborns and adults, and evaluated TLR- and CD40-mediated naïve B-cell class-switch recombination (CSR) and cytokine production. Gene expression levels of most TLRs was similar between newborn and adult B cells, except that newborn naïve B cells expressed more TLR9 than adult naïve B cells. Neonatal naïve B cells demonstrated impaired TLR2- and TLR7- but enhanced TLR9-mediated cytokine production. Significantly fewer newborn naïve B cells underwent CSR to produce IgG, an impairment also noted with IL-21 stimulation. Additionally, co-stimulation via CD40 and TLRs induced greater cytokine production in adult B cells. Thus, while newborn naïve B cells demonstrate adult-level expression of TLRs and CD40, the responses to stimulation of these receptors are distinct. Relatively high expression of TLR9 and impaired CD40-mediated Ig secretion contributes to distinct innate and adaptive immunity of human newborns and may inform novel approaches to early-life immunization.

Neonatal Fc Receptor-Mediated IgG Transport Across Porcine Intestinal Epithelial Cells: Potentially Provide the Mucosal Protection.

It has been well characterized that piglets can absorb colostrum IgG across the intestine to neonatal bloodstream and a certain level of IgG has been found in the mucosal secretions of the porcine intestinal tract. However, little is known about how the maternal IgG transport across the intestinal barrier and how IgG enter the lumen of intestinal tract. In this study, we demonstrated that the porcine neonatal Fc receptor (pFcRn) was expressed in a model of normal porcine intestinal epithelial cells (IPEC-J2) as well as in kidney cells (PK-15), and pFcRn was mainly distributed in the apical side of the polarized IPEC-J2 cells. Analyzing the phylogenetic relatedness of this gene we found that swine and human neonatal Fc receptor (FcRn) amino acid sequence are closer than rodents. We also showed that pFcRn mediated bidirectional IgG transport across polarized IPEC-J2 cells and bound to IgG in a pH-dependent manner. Furthermore, pFcRn-transcytosed viral-specific IgG reduced the transmissible gastroenteritis virus (TGEV) yield from the luminal direction by a 50% tissue culture infective dose (TCID50) assay. Our results indicate that pFcRn-dependent bidirectional IgG transport across the intestinal epithelium plays critical role in the acquisition of humoral immunity in early life and in host defense at mucosal surfaces.

Vitally important - does early innate immunity predict recruitment and adult innate immunity?

The immune system is one of the most important adaptations that has evolved to protect animals from a wide range of pathogens they encounter from early life onwards. During the early developmental period this is particularly true for the innate immunity, as other components of the immune system are, as yet, poorly developed. But innate immunity may not only be crucial for early life survival, but may also have long‐lasting effects, for example if early life immunity reflects the functioning of the immune system as a whole. For this reason, we investigated the importance of four constitutive innate immune parameters (natural antibodies, complement activity, concentrations of haptoglobin, and concentrations of nitric oxide) for recruitment in free‐living great tits. We compared nestling immunity of recruits with nestling immunity of their nonrecruited siblings. We also investigated within individual consistency of these innate immune parameters for those individuals that recruited, which may be taken as a measure of immune capacity. In accordance with previous studies, we found a clear effect of tarsus length and a trend for body mass on the likelihood to recruit. Nevertheless, we found no evidence that higher levels of constitutive innate immunity as a nestling facilitated local recruitment. Furthermore, individual innate immunity was not consistent across life stages, that is to say, nestling immune parameters did not determine, or respectively, reflect adult innate immune parameters. This plasticity in innate immune components may explain why we did not find long‐lasting survival benefits.