| First Author | Swanson RV | Year | 2023 |
| Journal | Nat Immunol | Volume | 24 |
| Issue | 5 | Pages | 855-868 |
| PubMed ID | 37012543 | Mgi Jnum | J:354107 |
| Mgi Id | MGI:7495986 | Doi | 10.1038/s41590-023-01476-3 |
| Citation | Swanson RV, et al. (2023) Antigen-specific B cells direct T follicular-like helper cells into lymphoid follicles to mediate Mycobacterium tuberculosis control. Nat Immunol 24(5):855-868 |
| abstractText | Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is a global cause of death. Granuloma-associated lymphoid tissue (GrALT) correlates with protection during TB, but the mechanisms of protection are not understood. During TB, the transcription factor IRF4 in T cells but not B cells is required for the generation of the T(H)1 and T(H)17 subsets of helper T cells and follicular helper T (T(FH))-like cellular responses. A population of IRF4(+) T cells coexpress the transcription factor BCL6 during Mtb infection, and deletion of Bcl6 (Bcl6(fl/fl)) in CD4(+) T cells (CD4(cre)) resulted in reduction of T(FH)-like cells, impaired localization within GrALT and increased Mtb burden. In contrast, the absence of germinal center B cells, MHC class II expression on B cells, antibody-producing plasma cells or interleukin-10-expressing B cells, did not increase Mtb susceptibility. Indeed, antigen-specific B cells enhance cytokine production and strategically localize T(FH)-like cells within GrALT via interactions between programmed cell death 1 (PD-1) and its ligand PD-L1 and mediate Mtb control in both mice and macaques. |
