Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice.

Cantor, Harvey; McVay-Boudreau, L; Hugenberger, J; Naidorf, Kenneth F.; Shen, Francis X.; Gershon, Richard K.

doi:10.1084/jem.147.4.1116

Cited by 257 publications

(94 citation statements)

References 13 publications

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“…There are three major ways to favor this skewing: (a) Pretreat the animals with a low dose of CY before their initial contact with antigen. CY, in the dose used, has been shown to inhibit cells in the suppressor T-cell circuit (11,12). Our results in this case contrast with the findings of Miller et al (13).…”

Section: Discussioncontrasting

confidence: 57%

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Ptak¹,

Różycka²,

Askenase³

et al. 1980

The Journal of Experimental Medicine

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156

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Three outcomes pertinent to contact sensitivity (CS) follow immunization with various forms of trinitrophenylated (TNP) substrates: (a) specific immunological unresponsiveness for CS is induced when immunization favors activation of splenic suppressor cells. This state is achieved by intravenous injection of trinitrophenyl-conjugated to various types of cells, such as peritoneal exudate cells (PEC). (b) A short-lived or evanescent form of CS is induced when immunization reduces activation of the suppressor circuit. This can be achieved by subcutaneous immunization with trinitrophenyl conjugated to syngeneic PEC, by pretreatment with cyclophosphamide to diminish suppression before intravenous immunization, or by altering the mode of antigen presentation by using TNP-substrate that has undergone phagocytosis. (c) A long-lived form of CS is induced when trinitrophenyl is presented to the immune system on skin cells either by contact skin painting with reactive trinitrophenyl, or by subcutaneous, or even intravenous injection of trinitrophenyl-conjugated epidermal cells. In fact, trinitrophenyl-conjugated epidermal cells induced CS even when the suppressor circuit was activated by intravenous coadministration of TNP-PEC. This implies that antigen presentation on epidermal cells induces sensitized cells that are relatively resistant to suppression. The cell type(s) in the skin that are primarily responsible for this potent form of antigen presentation are most likely Langerhans cells, because they can be concentrated by virtue of their Fc receptors and they are Ia positive. Thus, both the anatomical site where antigen is first encountered by the immune apparatus, as well as the nature of the cells which present the antigen, determine whether a CS response will ensue, as well as whether it will be evanescent or long-lasting.

show abstract

Section: Discussioncontrasting

confidence: 57%

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Ptak¹,

Różycka²,

Askenase³

et al. 1980

The Journal of Experimental Medicine

Self Cite

156

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show abstract

“…The suppressor cell precursor, the Ly 1 feedback inducer cell, the Ly 123 cell, or the mature suppressor cell could be regulated by androgens. Since many of these populations seem to be functionally or quantitatively abnormal in NZB mice (47,48), a defect in one or more could explain the lack of an androgen effect. Alternatively, androgens could act at the level of thymic epithelium or bone marrow T cell precursors in normal mice.…”

Section: (44)mentioning

confidence: 99%

Genetic studies in nzb mice

Raveché

Tjio

Steinberg

1980

Arthritis & Rheumatism

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Hybrid NZB X NZW or NZB X DBA/2 females have markedly accelerated development of autoimmunity when compared with their respective male littermates. This difference is attributable to the ability of male sex hormones to retard the expression of autoimmunity. In contrast to the sex differences in expression of autoimmunity in F1 mice, parental NZB males and females have only minor differences in disease expression. We have been investigating the basis for the difference in anti‐T cell antibody production between NZB and F1 mice. In this study, the appearance of antibodies cytotoxic for T cells (NTA) was studied in NZB and DBA/2 mice and in their F1 hybrids and backcross progeny. A major sex difference in NTA production was observed in the F1 hybrids; females produced more NTA than did males. Castration of males led to a marked increase in NTA production. Furthermore, the NTA production of castrated male and female F1 mice was significantly suppressed by administration of testosterone in Silastic capsules. In contrast to the studies in F1 mice, we found little difference between intact male and female parental NZB mice at any age studied. Furthermore, NZB mice of both sexes who were given androgen‐containing capsules at 2 weeks of age failed to demonstrate a decrease in NTA production. This result suggested an androgen insensitivity in NZB mice with regard to NTA production. This insensitivity, which appears to be a recessive trait, may help to explain why NZB mice do not manifest the sex differences in disease expression observed in the F1 hybrids.

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“…This immunogenetic classification of T cells provides new criteria for investigating immunological disorders, because it can be determined serologically whether there are absolute or relative changes in the representation of Lyt sets, and whether these changes are associated with alterations in immune reactivity that correspond with the established functional properties of Lyt sets. For example, Cantor and colleagues (7) propose that NZB mice are prone to autoimmune disease because they are defective in feedback inhibition, this being reflected serologically in a deficiency in the Ly 123 population which is the source of suppressor T cells.…”

mentioning

confidence: 99%

Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice.

Reske‐Kunz¹,

Scheid²,

Boyse³

1979

The Journal of Experimental Medicine

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Mice of the HRS strain, which carry the mutant gene hr, were examined for abnormalities in representation of the three T-cell sets Ly1, Ly23, and Ly123 in the spleen. The salient feature of hr/hr mice, which are immunologically deficient, in comparison with +/hr segregants, was a gross disproportion in numbers of cells belonging to the Ly1 and Ly123 sets, at the age of 3--3.5 mo. At this age, Ly123 cells of hr/hr spleen outnumbered Ly1 cells by 2:1, whereas in +/hr spleens Ly123 cells were outnumbered by approximately 1:2. Cells from pooled lymph nodes of hr/hr mice did not show a correspondingly gross disporprotion of Ly1 and Ly123 cells. Total counts of splenic T cells, and of B cells, were not significantly different in hr/hr and +/hr mice.

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Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice.

Cited by 257 publications

References 13 publications

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Role of antigen-presenting cells in the development and persistence of contact hypersensitivity.

Genetic studies in nzb mice

Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice.

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