T cell suppression of contact sensitivity in the mouse. II. The role of soluble suppressor factor and its interaction with macrophages

Zembala, Marek; Asherson, G. L.

doi:10.1002/eji.1830041206

Cited by 127 publications

(45 citation statements)

References 17 publications

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“…The starting point of this paper was the observation that the lymph node and spleen cells of mice injected with picrylsulphonic acid and then painted with the correspond ing antigen (picryl chloride) produce an a-pi cryl T suppressor factor (TSF) in vitro [1,2], This factor arms peritoneal exudate cells in suspension which then release a distinct nonspecific factor when exposed to antigen. This in turn depresses the passive transfer of contact sensitivity by immune cells incu bated in it and is nonspecific in its action [3], This paper shows that the cell in the peritoneal exudate which generates this fac tor is adherent and theta-negative and be longs, in all probability, to the monocytemacrophage series.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of Contact Sensitivity by Macrophages

Ptak

Zembala

Asherson

et al. 1981

Int Arch Allergy Immunol

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Lymphoid cells of mice injected with picrylsulphonic acid and then painted with picryl chloride produce a specific T suppressor factor (TSF) in vitro. This factor arms peritoneal exudate cells, which then produce a nonspecific factor which inhibits the transfer of contact sensitivity by immune cells incubated in it. An adherent, theta-negative cell, which is presumably a macrophage, is responsible. This justifies the use of the term macrophage suppressor factor. As a separate phenomenon, passive transfer cells lose their activity when incubated on high density monolayers of normal peritoneal exudate cells. However, this is not associated with the production of a supernatant factor. The inhibition of transfer when immune cells are incubated with specific TSF is unaffected by nylon wool filtration (which removes macrophages). This suggests that TSF is able to depress the passive transfer of contact sensitivity by a macrophage-independent process.

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Section: Discussionmentioning

confidence: 99%

“…T cells from mice injected with picrylsul phonic acid make a specific T cell suppres sor factor iu vitro [1,2]. This factor inhibits the passive transfer of contact sensitivity by immune cells incubated in it.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Contact Sensitivity by Macrophages

Ptak

Zembala

Asherson

et al. 1981

Int Arch Allergy Immunol

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“…There are several examples of soluble T-cell factors that influence the magnitude and quality of the immune response (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). Thus, the above findings prompted us to explore the subcellular component of T cells which can mediate the antigen-specific suppression of the antibody response .…”

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confidence: 99%

Properties of antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. I. In vivo activity and immunochemical characterization.

Takemori¹,

Tada²

1975

The Journal of Experimental Medicine

170

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Our previous publications (1, 2) indicated that thymocytes and spleen cells of mice that had been immunized with a high dose of carrier antigen, when transferred into syngeneic host, could suppress the antibody response against a hapten coupled to the homologous carrier . This suppressive effect was found to be mediated by a population of thymus-derived lymphocytes, whose activity was completely abrogated by the treatment with anti-B and complement . Moreover, the specificity of the observed suppression has been established by the fact that neither normal T cells nor those obtained from mice immunized with an unrelated antigen could suppress the antibody response . These results indicate that immunization with a relatively high dose of carrier antigen generated a subpopulation of T cells that specifically inhibits the antibody response against hapten on the same carrier. Similar antigen-specific T-cell-mediated suppression has recently been demonstrated in a number of other experimental systems (3-10), and is now considered to be an important regulatory mechanism in various forms of immune responses (reviewed in 11).A possible molecular mechanism of the antigen-specific suppression is that certain primed T cells liberate a suppressive factor(s) which then gives rise to an "off" signal to other cell types via combination with antigen. There are several examples of soluble T-cell factors that influence the magnitude and quality of the immune response (12-24). Thus, the above findings prompted us to explore the subcellular component of T cells which can mediate the antigen-specific suppression of the antibody response . We have attempted to separate such a soluble component by simple sonication followed by ultracentrifugation of the thymocytes and spleen cells possessing the suppressor activity, since we were successful in obtaining an antigen-specific suppressive factor from sonicated Tcells of the rat, which had shown a strong inhibitory effect on an ongoing IgE antibody response of the same species (19,25) . This paper will describe some of the properties of the antigen-specific suppressive T-cell factor obtained in mice, which was found to suppress mainly IgG antibody response of syngeneic mice in an in vivo experimental system .

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“…pretreatment with TNP-thymocytes, or OX-MRBC, respectively. This treatment induces in these animals an in vivo state of antigen-specific unresponsiveness, known to be mediated by suppressive T cells [35]. The results in Fig.…”

Section: Heat Aggregated Ig Protective Activity In Vivo Is Directed Imentioning

confidence: 79%

Aggregated Immunoglobulin Protects Immune T Cells from Suppression: Dependence on Isotype, Fc Portion, and Macrophage FcγR

et al. 1998

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We determined the regulatory properties of heat‐aggregated immunoglobulins (HA‐Ig) that possess many activities of immune complexes (IC), such as binding and activation of cells via immunoglobulin Fc γ receptors (FcγR). HA‐Ig protected contact sensitivity (CS) effector T cells from antigen‐specific immunosuppression, while monomeric IgG were inactive. This anti‐suppressive activity of HA‐Ig was antigen non‐specific, and depended on the species from which Ig was derived, i.e. mouse and rat HA‐Ig were protective in mice, and of other species were inactive. The protecting activity of HA‐Ig was confined to IgG2a and IgG3, and to a lesser degree to IgG1 isotypes, and resided in the Fc domain. Removal of phagocytic cells from the CS‐immune target cells, or blocking with anti‐FcγR mAb, abolished HA‐Ig protection of CS‐effector T cells from suppression. We suggest that HA‐Ig multimers acted via Fc domains, in one of two ways: by binding to FcγR of macrophages to produce positive‐acting cytokines, or by blocking FcγR on macrophages, to compete with suppressive factors that can also bind to FcγR. If HA‐Ig protection of T cells is generalized, it is likely that IC in vivo may non‐specifically overcome suppression of responses to antigen that normally are under the control of T suppressive cells, and thus may contribute to the development of autoimmunity.

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T cell suppression of contact sensitivity in the mouse. II. The role of soluble suppressor factor and its interaction with macrophages

Cited by 127 publications

References 17 publications

Inhibition of Contact Sensitivity by Macrophages

Inhibition of Contact Sensitivity by Macrophages

Properties of antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. I. In vivo activity and immunochemical characterization.

Aggregated Immunoglobulin Protects Immune T Cells from Suppression: Dependence on Isotype, Fc Portion, and Macrophage FcγR

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