Epirestriction and a Specialized Subset of T Helper Cells Are Key Factors in the Regulation of T Suppressor Cells

Mitchison, N. A.; Oliveira, D. B. G.

doi:10.1016/b978-0-12-174685-8.50035-4

Cited by 7 publications

(2 citation statements)

References 37 publications

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“…16|. Mitchison & Oliveira [17] have argued that ihcsc observations suggest a strong bias for suppressivc responses to be restricted to I-E. As a large iitimber of mice are I-E negative. they suggest that in the absence of 1-H molecules.…”

Section: Discussionmentioning

confidence: 99%

The Influence of I‐E on the Generation of Autoantibody and Specific Suppression in Rat Erythrocyte‐Immunized Mice

Elliott¹,

Cooke

1992

Scand J Immunol

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A proportion of the antibodies produced by mice in response to the injection of rat erythrocytes (RRBC) cross-react with autologous red cells. When spleen cells from mice so immunized are transferred to naive syngeneic recipients, the recipient mice produce high anti-RRBC antibody titres but little or no autoantibody. This phenomenon has been attributed to the action of suppressor T cells. To date, the only mouse strain which consistently fails to demonstrate specific suppression of the autoantibody response is the SJL, which lacks the I-E molecules suggested to be important in the generation of suppressor T cells. The results presented here show that some, but not all, I-E negative strains of mice are capable of exhibiting transferable suppression of RRBC-induced antibodies.

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Section: Discussionmentioning

confidence: 99%

The Influence of I‐E on the Generation of Autoantibody and Specific Suppression in Rat Erythrocyte‐Immunized Mice

Elliott¹,

Cooke

1992

Scand J Immunol

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“…Opinions among immunologists vary from those who regard this cell as playing a fundamental role in regulation of the immune response, to those who regard it as no more than an illusion. My own opinion, expressed in several recent and forthcoming reviews [4][5][6][7], lies somewhere between these two poles. I think it likely that a suppressor mechanism does operate, and that it has evolved primarily as a measure to counteract that threat of hypersensitivity.…”

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confidence: 99%

Logical Structure of the Immunoregulatory Compartment

Mitchison

1989

Haematology and Blood Transfusion / Hämatologie Und Bluttransfusion

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A genetically determined lack of oral tolerance to ovalbumin is due to failure of the immune system to respond to intestinally derived tolerogen

1987

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In this study we have examined whether differences between mouse strains in the induction of tolerance after feeding ovalbumin (OVA) are due to differences in intestinal processing of OVA or are determined by the systemic immune system. Compared with major histocompatibility complex (MHC)-congenic BALB/c mice, BALB/B mice develop much less tolerance of systemic delayed-type hypersensitivity (DTH) and humoral immunity after feeding OVA and this defect is also expressed partially in (BALB/B x BALB/c)F1 animals. Serum taken from either BALB/c or BALB/B mice fed OVA 1 h before produced significant suppression of systemic DTH responses in BALB/c, but not in BALB/B mice. Although OVA-fed BALB/B serum was slightly less tolerogenic than BALB/c serum, we conclude that the defective induction of oral tolerance in BALB/B mice is due primarily to a MHC-influenced defect with the immune system. These findings support the idea that clinical food-sensitive enteropathy reflects an immune response gene-controlled defect in tolerance to dietary proteins.

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Epirestriction and a Specialized Subset of T Helper Cells Are Key Factors in the Regulation of T Suppressor Cells

Cited by 7 publications

References 37 publications

The Influence of I‐E on the Generation of Autoantibody and Specific Suppression in Rat Erythrocyte‐Immunized Mice

The Influence of I‐E on the Generation of Autoantibody and Specific Suppression in Rat Erythrocyte‐Immunized Mice

Logical Structure of the Immunoregulatory Compartment

A genetically determined lack of oral tolerance to ovalbumin is due to failure of the immune system to respond to intestinally derived tolerogen

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