ArticleImmunology2009
Beta(2) integrin deficiency yields unconventional double-negative T cells distinct from mature classical natural killer T cells in mice.
Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- β2 Integrins differentially regulate γδ T cell subset thymic development and peripheral maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Double-negative T resident memory cells of the lung react to influenza virus infection via CD11c(hi) dendritic cells.Mucosal immunology · 2016Article
- T cell-extrinsic CD18 attenuates antigen-dependent CD4+ T cell activation in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Hematopoietic stem/progenitor cells directly contribute to arteriosclerotic progression via integrin β2.Stem cells (Dayton, Ohio) · 2015Article
- The integrin adhesome: from genes and proteins to human disease.Nature reviews. Molecular cell biology · 2014Review
- Adaptive immune response to model antigens is impaired in murine leukocyte-adhesion deficiency-1 revealing elevated activation thresholds in vivo.Clinical & developmental immunology · 2012Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expressed on leucocytes, beta(2) 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-alphabeta (TCR-alphabeta) and TCR-gammadelta 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 CD18(wt) recipients but, like antigen-experienced T or natural killer (NK) T cells, recirculated through non-lymphoid organs. Lacking regulatory functions in vitro, CD18(-/-) TCR-alphabeta DN T cells did not suppress the proliferation of polyclonally activated CD4(+) or CD8(+) (single-positive; SP) T cells. Most interestingly, CD18(-/-) TCR-alphabeta 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-alphaGalCer dimers, these cells are not mature classical NKT cells. Our data indicate that CD18(-/-) TCR-alphabeta DN T cells, like NKT and TCR-gammadelta 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.
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