Two separate functions of class II (Ia) molecules: T-cell stimulation and B-cell excitation.

Corley, Ronald B.; Locascio, N. J.; Ovnic, Mariana; Haughton, Geoffrey

doi:10.1073/pnas.82.2.516

Cited by 42 publications

(14 citation statements)

References 26 publications

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“…Such up-regulation is characteristic of T cell activation (Corley et al 1985). It is widely assumed that clearance of viruses by the immune response requires virus-specific CD8 CTLs that destroy infected cells via cytotoxic granules such as perforin/granzymes or by death receptors and their specific ligand-dependent pathways (Guidotti & Chisari 2001).…”

Section: Table IIImentioning

confidence: 99%

Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Azeredo¹,

Zagne

Alvarenga³

et al. 2006

Mem. Inst. Oswaldo Cruz

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Section: Table IIImentioning

confidence: 99%

Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Azeredo¹,

Zagne

Alvarenga³

et al. 2006

Mem. Inst. Oswaldo Cruz

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“…Evidence for transduction of an activating signal by B-cell Ia molecules has come from a number of experimental systems. Differentiation of the murine B-cell lymphoma cell line CH12 to secretion of IgM was reported to require both (i) antigen reactive with CH12 cell surface immunoglobulin and (ii) T cells (1) or alloantibody reactive with I-E-encoded Ia molecules (2). Anti-class II MHC antibodies have been reported to stimulate proliferation and immunoglobulin secretion by pokeweed mitogen-treated B cells (3).…”

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confidence: 99%

Stimulation of B-cell proliferation by membrane-associated molecules from activated T cells.

Brian

1988

Proc. Natl. Acad. Sci. U.S.A.

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Activation of B cells to proliferation and antibody secretion is dependent on soluble lymphokines secreted by activated T cells. Activation of T cells results from physical contact between B cells and T cells through binding of the T-cell antigen receptor to a complex of antigen and class II major histocompatibility complex (MHC) molecules. To determine whether this interaction also contributes to B-cell activation by mechanisms other than those mediated by soluble T cell-derived lymphokines, I examined the ability of isolated T-cell plasma membranes to stimulate proliferation in cultures of unfractionated B cells. Membranes prepared from a cloned antigen-specific helper T-cell line induced substantial proliferation provided that the T cells had been mitogen-activated before isolation of membranes. Membranes from splenic Con A-treated blasts also stimulated B-cell proliferation, suggesting that this activity may be a common property of some subsets of activated T cells. Induction of B-cell proliferation was not found to be antigen-dependent or MHC-restricted, indicating no significant contribution by the T-cell receptor for antigen. The presence of interleukins 4 and 5 in membrane fractions was indicated by proliferation of lymphokinesensitive cell lines, although culture supernatants from mitogen-activated T cells proved to be far more potent sources of these activities. The combined effect of membranes and lymphokine-containing culture supernatants in B-cell cultures was greater than their added effects in separate cultures. This observation suggests that lymphokines or molecules with mitogenic activity for B cells other than those found in abundance in culture supernatants may be present on activated T-cell membranes.

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“…Corley et al (3) reported that the recognition of MHC class II-peptide complexes by specific T cell receptors (TCR) leads to the activation of both T lymphocytes and antigenpresenting cells (APCs), suggesting that MHC class II molecules can act as signal transducers. To confirm this possibility, anti-MHC class II antibodies (Abs) and superantigens (SAgs), which act as natural MHC class II ligands, were used to mimic MHC class II-peptide complex recognition by specific TCRs.…”

mentioning

confidence: 99%

Lipid Raft-dependent and -independent Signaling through HLA-DR Molecules

Bouillon¹,

Fakhry²,

Girouard³

et al. 2003

Journal of Biological Chemistry

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Lipid rafts are plasma membrane microdomains that are highly enriched in signaling molecules and that act as signal transduction platforms for many immune receptors. The involvement of these microdomains in HLA-DR-induced signaling is less well defined. We examined the constitutive presence of HLA-DR molecules in lipid rafts, their possible recruitment into these microdomains, and the role of these microdomains in HLA-DR-induced responses. We detected significant amounts of HLA-DR molecules in the lipid rafts of EBV ؉ and EBV ؊ B cell lines, monocytic cell lines, transfected HeLa cells, tonsillar B cells, and human monocytes. Localization of HLA-DR in these microdomains was unaffected by the deletion of the cytoplasmic domain of both the ␣ and ␤ chains. Ligation of HLA-DR with a bivalent, but not a monovalent, ligand resulted in rapid tyrosine phosphorylation of many substrates, especially Lyn, and activation of ERK1/2 MAP kinase. However, the treatment failed to induce further recruitment of HLA-DR molecules into lipid rafts. The HLA-DR-induced signaling events were accompanied by the induction of cellcell adhesion that could be inhibited by PTK and Lyn but not ERK1/2 inhibitors. Disruption of lipid rafts by methyl-␤-cyclodextrin (M␤CD) resulted in the loss of membrane raft association with HLA-DR molecules, inhibition of HLA-DR-mediated protein tyrosine phosphorylation and cell-cell adhesion. M␤CD did not affect the activation of ERK1/2, which was absent from lipid rafts. These results indicate that although all the HLA-DRinduced events studied are dependent on HLA-DR dimerization, some require the presence of HLA-DR molecules in lipid rafts, whereas others do not. Although major histocompatibility complex (MHC)1 class II molecules do not possess any known signaling motifs in their cytoplasmic and transmembrane domains, they act as signal transducers in addition to playing a critical role in antigen presentation and autoimmune disease susceptibility and severity (1, 2). Corley et al. (3) reported that the recognition of MHC class II-peptide complexes by specific T cell receptors (TCR) leads to the activation of both T lymphocytes and antigenpresenting cells (APCs), suggesting that MHC class II molecules can act as signal transducers. To confirm this possibility, anti-MHC class II antibodies (Abs) and superantigens (SAgs), which act as natural MHC class II ligands, were used to mimic MHC class II-peptide complex recognition by specific TCRs. This ligation led to various cellular events such as homotypic and heterotypic cell-cell adhesion (4), B cell proliferation and differentiation (5), cytokine production, and expression of costimulatory molecules (6) and, under certain conditions, cell death (7). Like other ligand-receptor interactions, some of these events are dependent on MHC class II ligand dimerization (8, 9), generate cAMP and intracellular calcium flux (1), and are mediated by signaling pathways and secondary messengers including protein kinase C (PKC), protein tyrosine kinase (PTK), cyclooxygenase 2,...

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Two separate functions of class II (Ia) molecules: T-cell stimulation and B-cell excitation.

Cited by 42 publications

References 26 publications

Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Stimulation of B-cell proliferation by membrane-associated molecules from activated T cells.

Lipid Raft-dependent and -independent Signaling through HLA-DR Molecules

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