Contrasting Requirements for IL-2 Production, IL-2 Receptor Expression, and Lymphocyte Proliferation: The Role of Calcium-Dependent and Calcium-Independent Signals

Gelfand, Erwin W.; Mills, Gordon B.; Cheung, Roy K.; Lee, Jacob W.; Grinstein, Sergio

doi:10.1016/b978-0-12-432014-7.50010-3

Cited by 10 publications

(1 citation statement)

References 61 publications

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“…Activation of PKC and increase in [Ca2+]i are two of the early events of T cell activation [22]. Since phorbol ester activates PKC, the results in Table 5 reaches its peak value in 2-3 min, though at times it rises steadily for several minutes (Fig.…”

Section: Class I Ag Mobilize Cytoplasmic Calcium In T Cells and Elevamentioning

confidence: 95%

Involvement of major histocompatibility complex class I antigens in T cell activation

et al. 1990

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During the last few years ample evidence has been collected indicating a regulatory role for major histocompatibility complex class I antigens (Ag) in T cell activation. However, due to differential effects (stimulatory and inhibitory) of anti-class I antibodies (Ab) observed under different conditions, no coherent scheme of the mechanism of action of these Ag has emerged. Here, we present evidence that the mode of action of anti-class I Ab depends upon the presence or absence of monocytes/macrophages (M phi) in the culture. The Ab inhibit Ag presentation by binding to M phi. Coating of tetanus toxin -pulsed M phi with anti-class I Ab is sufficient to suppress T cell activation. On the contrary, these Ab enhance lectin- as well as phorbol ester-induced T cell activation in the absence of M phi. Cross-linking of class I Ag on T cell surface mobilizes cytoplasmic Ca2+, and also enhances the CD3-induced Ca2+ flux inside the cells indicating a functional relationship between CD3 and class I Ag. Though surface modulation and immunoprecipitation experiments do not indicate any physical association between these two types of molecules on the T cell surface, capping studies show that cross-linking of class I Ag induces an association of these Ag with CD3. Binding of anti-CD3 Ab enhances the strength of association between CD3 and class I Ag, and the former co-caps completely with the latter. Based on these observations we propose that during antigen presentation M phi (or Ag-presenting cells) and T cells, besides interacting via peptide--class II Ag/CD3--T cell receptor complex formation, also interact through class I Ag. The latter interaction may stabilize the contact formation between T cells and Ag-presenting cell and support T cell activation.

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Section: Class I Ag Mobilize Cytoplasmic Calcium In T Cells and Elevamentioning

confidence: 95%

Involvement of major histocompatibility complex class I antigens in T cell activation

et al. 1990

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Phenotypic Features of Selective T Cell Deficiency Characterized by Absence of CD8+T Lymphocytes and Undetectable mRNA for ZAP-70 Kinase

Mazer

Harbeck

Franklin

et al. 1997

Clinical Immunology and Immunopathology

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Activation signals in human lymphocytes: Interleukin 2 synthesis and expression of high affinity interleukin 2 receptors require differential signalling for the activation of protein kinase C

Szamel

Kracht

Krebs

et al. 1990

Cellular Immunology

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Contrasting Requirements for IL-2 Production, IL-2 Receptor Expression, and Lymphocyte Proliferation: The Role of Calcium-Dependent and Calcium-Independent Signals

Cited by 10 publications

References 61 publications

Involvement of major histocompatibility complex class I antigens in T cell activation

Involvement of major histocompatibility complex class I antigens in T cell activation

Phenotypic Features of Selective T Cell Deficiency Characterized by Absence of CD8+T Lymphocytes and Undetectable mRNA for ZAP-70 Kinase

Activation signals in human lymphocytes: Interleukin 2 synthesis and expression of high affinity interleukin 2 receptors require differential signalling for the activation of protein kinase C

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