Abstract
BackgroundIn the intestine, the integrin CD103 is expressed on a subset of T regulatory (Treg) cells and a population of dendritic cells (DCs) that produce retinoic acid and promote immune homeostasis. However, the role of CD103 during intestinal helminth infection has not been tested.Methodology/Principal FindingsWe demonstrate that CD103 is dispensable for the development of protective immunity to the helminth parasite Trichuris muris. While we observed an increase in the frequency of CD103+ DCs in the lamina propria (LP) following acute high-dose infection with Trichuris, lack of CD103 had no effect on the frequency of CD11c+ DCs in the LP or mesenteric lymph nodes (mLN). CD103-deficient (CD103−/−) mice develop a slightly increased and earlier T cell response but resolve infection with similar kinetics to control mice. Similarly, low-dose chronic infection of CD103−/− mice with Trichuris resulted in no significant difference in immunity or parasite burden. Absence of CD103 also had no effect on the frequency of CD4+CD25+Foxp3+ Treg cells in the mLN or LP.Conclusions/SignificanceThese results suggest that CD103 is dispensable for intestinal immunity during helminth infection. Furthermore, lack of CD103 had no effect on DC or Treg recruitment or retention within the large intestine.
Highlights
Mucosal sites such as the gastrointestinal and respiratory tracts are primary entry points for both innocuous and pathogenic agents, and multiple mechanisms control the balance between the development of immunity, regulation of inflammation and induction of tolerance [1]
Trichuris-specific serum IgG1 titers, a hallmark of systemic Th2 cell responses, were increased in CD1032/2 mice compared to infected WT mice, while IFN-c-dependent IgG2a titers were similar between WT and CD1032/2 mice (Figure 1B)
We demonstrate that CD103 is largely dispensable for large intestinal immune responses in vivo
Summary
Mucosal sites such as the gastrointestinal and respiratory tracts are primary entry points for both innocuous and pathogenic agents, and multiple mechanisms control the balance between the development of immunity, regulation of inflammation and induction of tolerance [1]. Within the gutassociated lymphoid tissues of the intestine, CD4+CD25+Foxp3+ regulatory T (Treg) cells and dendritic cells (DCs) are critical in the maintenance of mucosal immune homeostasis and subsets of these Treg cells and DCs express the E-cadherin receptor, aE(CD103)b7 integrin [2,3,4,5,6]. It has been suggested that CD103 is a critical component of intestinal immune homeostasis. CD103 plays a critical role in site-specific Treg cell retention in the skin under both resting conditions and following Leishmania major infection [8]. The integrin CD103 is expressed on a subset of T regulatory (Treg) cells and a population of dendritic cells (DCs) that produce retinoic acid and promote immune homeostasis. The role of CD103 during intestinal helminth infection has not been tested
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