Abstract
A myriad of pathogens gain access to the host via the mucosal route; thus, vaccinations that protect against mucosal pathogens are critical. Pathogens such as HIV, HSV, and influenza enter the host at mucosal sites such as the intestinal, urogenital, and respiratory tracts. All currently licensed vaccines mediate protection by inducing the production of antibodies which can limit pathogen replication at the site of infection. Unfortunately, parenteral vaccination rarely induces the production of an antigen-specific antibody at mucosal surfaces and thus relies on transudation of systemically generated antibody to mucosal surfaces to mediate protection. Mucosa-associated lymphoid tissues (MALTs) consist of a complex network of immune organs and tissues that orchestrate the interaction between the host, commensal microbes, and pathogens at these surfaces. This complexity necessitates strict control of the entry and exit of lymphocytes in the MALT. This control is mediated by chemoattractant chemokines or cytokines which recruit immune cells expressing the cognate receptors and adhesion molecules. Exploiting mucosal chemokine trafficking pathways to mobilize specific subsets of lymphocytes to mucosal tissues in the context of vaccination has improved immunogenicity and efficacy in preclinical models. This review describes the novel use of MALT chemokines as vaccine adjuvants. Specific attention will be placed upon the use of such adjuvants to enhance HIV-specific mucosal humoral immunity in the context of prophylactic vaccination.
Highlights
Many pathogens access the host via mucosal barrier surfaces
The mucosa-associated lymphoid tissues (MALTs) are an interactive network of organs and tissues that are responsible for the education of mucosal lymphocytes and the orchestration of responses against commensal microbes and pathogens
Activated lymphocytes are rarely able to traffic to mucosal sites due to low, or lack of expression, specific adhesion and chemokine receptors required for entry into these sites
Summary
Many pathogens access the host via mucosal barrier surfaces. developing vaccines that elicit robust effector and memory responses at mucosal sites is a crucial public health goal. The trial demonstrated efficacy ranging from 26.4%–31% It was determined after analysis of patient samples that protection correlated with HIV-specific serum IgG which mediated antibody-dependent cellular cytotoxicity (ADCC). While analysis from RV144 trial vaccinees indicated that serum IgA positively correlated with infection risk, Sholukh and colleagues found that the combination of dIgA and IgG (targeting the same HGN194 (a neutralizing epitope in env)), applied intrarectally, led to 100% protection from intrarectal challenge [14]. These results suggest different roles for serum IgA and mucosal dIgA. The potential role of mucosal IgA in mediating protection from HIV infection necessitates a clear understanding of the function of inductive and effector mucosal immune organs, as IgA-secreting B cells are induced and educated at these sites
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