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- Title
β<sub>2</sub> Integrin deficiency yields unconventional double-negative T cells distinct from mature classical natural killer T cells in mice.
- Authors
Oreshkova, Tsvetelina; Wang, Honglin; Seier, Anne M.; Sindrilaru, Anca; Varga, Georg; Grabbe, Stephan; Scharffetter-Kochanek, Karin; Peters, Thorsten
- Abstract
Expressed on leucocytes, β2 integrins (CD11/CD18) are specifically involved in leucocyte function. Using a CD18-deficient (CD18−/−) mouse model, we here report on their physiological role in lymphocyte differentiation and trafficking. CD18−/− mice present with a defect in the distribution of lymphocytes with highly reduced numbers of naïve B and T lymphocytes in inguinal and axillary lymph nodes. In contrast, cervical lymph nodes were fourfold enlarged harbouring unconventional T-cell receptor-αβ (TCR-αβ) and TCR-γδ CD3+ CD4− CD8− (double-negative; DN) T cells that expanded in situ. Using adoptive transfer experiments, we found that these cells did not home to peripheral lymph nodes of CD18wt recipients but, like antigen-experienced T or natural killer (NK) T cells, recirculated through non-lymphoid organs. Lacking regulatory functions in vitro, CD18−/− TCR-αβ DN T cells did not suppress the proliferation of polyclonally activated CD4+ or CD8+ (single-positive; SP) T cells. Most interestingly, CD18−/− TCR-αβ DN T cells showed intermediate TCR expression levels, an absent activation through allogeneic major histocompatibility complex and a strong proliferative dependence on interleukin-2, hence, closely resembling NKT cells. However, our data oppose former reports, clearly showing that, because of an absent reactivity with CD1d-αGalCer dimers, these cells are not mature classical NKT cells. Our data indicate that CD18−/− TCR-αβ DN T cells, like NKT and TCR-γδ T cells, share characteristics of both adaptive and innate immune cells, and may accumulate as a compensatory mechanism to the functional defect of adaptive immunity in CD18−/− mice.
- Subjects
GENE expression; LEUCOCYTES; T cells; KILLER cells; LABORATORY mice
- Publication
Immunology, 2009, Vol 128, Issue 2, p271
- ISSN
0019-2805
- Publication type
Article
- DOI
10.1111/j.1365-2567.2009.03116.x