T lymphocytes in acute bacterial infection: increased prevalence of CD11b super(+) cells in the peripheral blood and recruitment to the infected site
T-cell activation, particularly of CD8 super(+) cells, is invariably associated with viral infections. We now provide evidence for the activation of T cells in patients with localized bacterial soft tissue infections. During acute disease we detected in the peripheral blood of these patients, small...
Saved in:
Published in | Immunology Vol. 125; no. 4; pp. 503 - 509 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
01.12.2008
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | T-cell activation, particularly of CD8 super(+) cells, is invariably associated with viral infections. We now provide evidence for the activation of T cells in patients with localized bacterial soft tissue infections. During acute disease we detected in the peripheral blood of these patients, small though conspicuous populations of CD4 super(+)CD28 super(+)CD11b super(+) and CD8 super(+)CD28 super(+)CD11b super(+) cells, indicative of an expansion of effector T cells. Moreover, we identified CD4 super(+) and CD8 super(+) cells at the infected site, in addition to highly activated polymorphonuclear neutrophils (PMN). In keeping with their role as first-line defence, PMN were preponderant, but T cells amounted to 20% of the infiltrated cells. The majority of the infiltrated T cells expressed CXCR6, a homing receptor for non-lymphoid tissue. The infiltrated T cells produced interferon-g (IFN-g), while the peripheral blood cells obtained at the same time did not. In conclusion, in response to localized bacterial infections, T cells are activated and recruited to the infected site. We propose that these T cells, e.g. by producing IFN-g, enhance the efficiency of the infiltrated phagocytic cells, particularly of the PMN, thereby supporting the local host defence. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 content type line 23 ObjectType-Feature-2 |
ISSN: | 0019-2805 1365-2567 |
DOI: | 10.1111/j.1365-2567.2008.02863.x |