Abstract
Viruses form particulate structures possessing high-density B-cell epitopes and viral RNA/DNA, which are ligands for multiple Toll-like receptors (TLRs). B cells are able to sense these viral antigenic signatures through B-cell antigen receptors (BCRs) and TLRs, both of which synergistically shape the magnitude and quality of virus-specific B-cell responses. In many viruses, B-cell recognition of these virus signatures is often hampered by tissue tropisms toward nonlymphoid organs. However, ectopic localizations of B cells at virus replication sites facilitate the efficient recognition of intact virus particles. Following pulmonary infection by influenza virus, virus-specific B-cell responses occur in the tertiary lymphoid organs of lungs near the sites of virus replication as well as in the draining lymph nodes. Lungs then begin to support the germinal center response and the formation of niches for plasma cells and memory B cells, thus potentiating B-cell intrinsic recognition of virus particles at these sites. In this review, we discuss how the anatomical location and virus- sensing properties of B cells coordinate protective B-cell responses against pulmonary virus infection.
Keywords: Affinity maturation, germinal center, influenza virus, lung, memory B cell, plasma cell, toll-like receptor, B-cell epitopes, toll-like receptor, viral RNA/DNA, plasma cells, viral antigenic, anatomical location, pulmonary virus infection, immune response, pathogen
Infectious Disorders - Drug Targets
Title:Primary and Secondary B-Cell Responses to Pulmonary Virus Infection
Volume: 12 Issue: 3
Author(s): Yoshimasa Takahashi, Taishi Onodera, Kazuo Kobayashi and Tomohiro Kurosaki
Affiliation:
Keywords: Affinity maturation, germinal center, influenza virus, lung, memory B cell, plasma cell, toll-like receptor, B-cell epitopes, toll-like receptor, viral RNA/DNA, plasma cells, viral antigenic, anatomical location, pulmonary virus infection, immune response, pathogen
Abstract: Viruses form particulate structures possessing high-density B-cell epitopes and viral RNA/DNA, which are ligands for multiple Toll-like receptors (TLRs). B cells are able to sense these viral antigenic signatures through B-cell antigen receptors (BCRs) and TLRs, both of which synergistically shape the magnitude and quality of virus-specific B-cell responses. In many viruses, B-cell recognition of these virus signatures is often hampered by tissue tropisms toward nonlymphoid organs. However, ectopic localizations of B cells at virus replication sites facilitate the efficient recognition of intact virus particles. Following pulmonary infection by influenza virus, virus-specific B-cell responses occur in the tertiary lymphoid organs of lungs near the sites of virus replication as well as in the draining lymph nodes. Lungs then begin to support the germinal center response and the formation of niches for plasma cells and memory B cells, thus potentiating B-cell intrinsic recognition of virus particles at these sites. In this review, we discuss how the anatomical location and virus- sensing properties of B cells coordinate protective B-cell responses against pulmonary virus infection.
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Cite this article as:
Takahashi Yoshimasa, Onodera Taishi, Kobayashi Kazuo and Kurosaki Tomohiro, Primary and Secondary B-Cell Responses to Pulmonary Virus Infection, Infectious Disorders - Drug Targets 2012; 12 (3) . https://dx.doi.org/10.2174/187152612800564400
DOI https://dx.doi.org/10.2174/187152612800564400 |
Print ISSN 1871-5265 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3989 |
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