tetano
Editor, Senior Moderator
Infect Disord Drug Targets. 2012 Mar 6. [Epub ahead of print]
Primary and Secondary B-Cell Responses to Pulmonary Virus Infection.
Takahashi Y, Onodera T, Kobayashi K, Kurosaki T.
Source
Department of Immunology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku, Tokyo 162-8640, Japan. ytakahas@nih.go.jp.
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.
PMID:
22394179
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22394179
Primary and Secondary B-Cell Responses to Pulmonary Virus Infection.
Takahashi Y, Onodera T, Kobayashi K, Kurosaki T.
Source
Department of Immunology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku, Tokyo 162-8640, Japan. ytakahas@nih.go.jp.
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.
PMID:
22394179
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22394179