| First Author | Malaviarachchi PA | Year | 2020 |
| Journal | Eur J Immunol | Volume | 50 |
| Issue | 5 | Pages | 676-684 |
| PubMed ID | 32026472 | Mgi Jnum | J:288851 |
| Mgi Id | MGI:6416354 | Doi | 10.1002/eji.201948391 |
| Citation | Malaviarachchi PA, et al. (2020) Antibody, but not B-cell-dependent antigen presentation, plays an essential role in preventing Chlamydia systemic dissemination in mice. Eur J Immunol 50(5):676-684 |
| abstractText | The obligate intracellular bacterium Chlamydia trachomatis causes the most prevalent bacterial sexually transmitted infection worldwide. CD4 T cells play a central role in the protective immunity against Chlamydia female reproductive tract (FRT) infection, while B cells are thought to be dispensable for resolution of primary Chlamydia infection in mouse models. We recently reported an unexpected requirement of B cells in local Chlamydia-specific CD4 T-cell priming and bacterial containment within the FRT. Here, we sought to tackle the precise effector function of B cells during Chlamydia primary infection. Using mixed bone marrow chimeras that lack B-cell-dependent Ag presentation (MHCII(B) - / - ) or devoid of circulating antibodies (AID(-/-) x muS(-/-) ), we show that Chlamydia-specific CD4 T-cell expansion does not rely on Ag presentation by B cells. Importantly, we demonstrate that antibody, but not B-cell-dependent Ag presentation, is required for preventing systemic bacterial dissemination following Chlamydia FRT infection. |
