Histological features of skin reactions to human lymphoid cell line lymphokine in patients with advanced cancer

Dumonde, D. C.; Pulley, Melanie S.; Paradinas, F. J.; Southcott, Barbara M.; O'Connell, Daniel; Robinson, M. R. G.; Hollander, Frank den; Schuurs, A.H.W.M.

doi:10.1002/path.1711380402

Cited by 25 publications

(10 citation statements)

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“…ϩ T cells inducing proliferation of memory T cells (46) and play an important role in grafting of transplants (54) as well as in presenting recall antigens in human delayed hypersensitivity reactions (13,46). In this regard, inhibition of caveolin-1 and CD26 interaction in the human system may provide a significant treatment strategy not only for the inflammatory state but also for transplantation.…”

Section: Discussionmentioning

confidence: 99%

CD26 Mediates Dissociation of Tollip and IRAK-1 from Caveolin-1 and Induces Upregulation of CD86 on Antigen-Presenting Cells

Ohnuma

Yamochi

Uchiyama

et al. 2005

Molecular and Cellular Biology

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CD26 is a T-cell costimulatory molecule with dipeptidyl peptidase IV enzyme activity in its extracellular region. We have previously reported that the addition of recombinant soluble CD26 resulted in enhanced proliferation of human T lymphocytes induced by the recall antigen tetanus toxoid (TT) via upregulation of CD86 on monocytes and that caveolin-1 was a binding protein of CD26, and the CD26-caveolin-1 interaction resulted in caveolin-1 phosphorylation (p-cav-1) as well as TT-mediated T-cell proliferation. However, the mechanism involved in this immune enhancement has not yet been elucidated. In the present work, we perform experiments to identify the molecular mechanisms by which p-cav-1 leads directly to the upregulation of CD86. Through proteomic analysis, we identify Tollip (Toll-interacting protein) and IRAK-1 (interleukin-1 receptorassociated serine/threonine kinase 1) as caveolin-1-interacting proteins in monocytes. We also demonstrate that following stimulation by exogenous CD26, Tollip and IRAK-1 dissociate from caveolin-1, and IRAK-1 is then phosphorylated in the cytosol, leading to the upregulation of CD86 via activation of NF-B. Binding of CD26 to caveolin-1 therefore regulates signaling pathways in antigen-presenting cells to induce antigenspecific T-cell proliferation.CD26 is a widely distributed 110-kDa cell surface glycoprotein with known dipeptidyl peptidase IV (DPPIV) (EC 3.4.14.5) activity in its extracellular domain (16,38). This enzyme is capable of cleaving amino-terminal dipeptides with either L-proline or L-alanine at the penultimate position. While CD26 expression is enhanced following activation of resting T cells, CD4 ϩ CD26 high T cells respond maximally to recall antigens such as tetanus toxoid (TT) (39). Cross-linking of CD26 and CD3 with solid-phase immobilized monoclonal antibodies (MAbs) can induce T-cell costimulation and interleukin-2 (IL-2) production by either human CD4 ϩ T cells or Jurkat T-cell lines transfected with CD26 cDNA (16,56). In addition, anti-CD26 antibody treatment of T cells leads to a decrease in the surface expression of CD26 via its internalization, and such modulation results in an enhanced proliferative response to anti-CD3 or anti-CD2 stimulation as well as enhanced tyrosine phosphorylation of signaling molecules such as CD3 and p56-Lck (19). Moreover, we showed that DPPIV enzyme activity is required for CD26-mediated T-cell costimulation and various immune responses (23,45,58). We have recently shown that internalization of CD26 after cross-linking is mediated in part by the mannose-6-phosphate/insulin-like growth factor II receptor and that the interaction of CD26 and the mannose-6-phosphate/insulin-like growth factor II receptor plays a role in CD26-induced T-cell costimulation (20).In a recent study, we demonstrated that caveolin-1 is a binding protein of CD26 and that CD26 on activated memory T cells interacts with caveolin-1 on TT-loaded monocytes (43). In this interaction, the scaffolding domain (SCD) of caveolin-1, comprising residues 82 to 101...

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Section: Discussionmentioning

confidence: 99%

CD26 Mediates Dissociation of Tollip and IRAK-1 from Caveolin-1 and Induces Upregulation of CD86 on Antigen-Presenting Cells

Ohnuma

Yamochi

Uchiyama

et al. 2005

Molecular and Cellular Biology

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“…In humans, around four hours after Ag challenge neutrophils can be seen forming a "cuff" around the venules. This is followed by a dramatic influx of mononuclear cells, such that by 24 -48 h the lesion is mostly mononuclear with a mix of T cells and macrophages (73). Paradoxically, in mice where the peripheral blood has a relative paucity of neutrophils compared with humans, the DTH response tends to be more neutrophil rich (74).…”

Section: Differences In Immune System Biologymentioning

confidence: 99%

Of Mice and Not Men: Differences between Mouse and Human Immunology

Mestas

Hughes

2004

The Journal of Immunology

3,066

2,322

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Mice are the experimental tool of choice for the majority of immunologists and the study of their immune responses has yielded tremendous insight into the workings of the human immune system. However, as 65 million years of evolution might suggest, there are significant differences. Here we outline known discrepancies in both innate and adaptive immunity, including: balance of leukocyte subsets, defensins, Toll receptors, inducible NO synthase, the NK inhibitory receptor families Ly49 and KIR, FcR, Ig subsets, the B cell (BLNK, Btk, and λ5) and T cell (ZAP70 and common γ-chain) signaling pathway components, Thy-1, γδ T cells, cytokines and cytokine receptors, Th1/Th2 differentiation, costimulatory molecule expression and function, Ag-presenting function of endothelial cells, and chemokine and chemokine receptor expression. We also provide examples, such as multiple sclerosis and delayed-type hypersensitivity, where complex multicomponent processes differ. Such differences should be taken into account when using mice as preclinical models of human disease.

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“…The same endothelial changes are ob served in delayed hypersensitivity reactions [66,79,163] and in skin lesions induced by intradermal injection of mixed Iymphokines [64], The initial infiltrate in delayed hyper sensitivity reactions is enriched for antigenspecific T cells [189]. Lymphocytes and lym phoblasts, some in mitosis, are seen attached to the lumens of venules and in perivenular 'cuffs' [67], Microvessel endothelial cells with HEV phenotype are also found in nor mal lymph nodes.…”

Section: Lymphocyte Adherencementioning

confidence: 95%