Preventive Effect of Hapten-Reactive Thymus-Derived Helper Lymphocytes on the Tolerance Induction in Hapten-Specific Precursors of Antibody-Forming Cells

Hamaoka, Toshiyuki; Inada, Tetsushi; Yamashita, Uki; Kitagawa, Masayoshi

doi:10.4049/jimmunol.114.6.1771

Cited by 8 publications

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Secondary IgG responses to type 3 pneumococcal polysaccharide III. T cell requirement for development of B memory

Braley‐Mullen

1977

Eur J Immunol

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Mice primed with a thymus-dependent form of Type 3 pneumococcal polysaccharide (S3), i.e. S3 coupled to erythrocytes (S3-RBC) produces S3-specific IgG antibody after secondary challenge with S3-RBC. When mice are depleted of T cells by treatment with anti-lymphocyte serum (ALS) at the time of priming, no IgG antibody is produced after secondary challenge. In order to determine the cellular basis for this phenomenon, various combinations of T and/or B cells from ALS-treated or normal primed mice were transferred to irradiated recipients prior to secondary challenge with S3-RBC. The results indicated that T cells were required at the time of priming with S3-RBC in order to (a) prevent the induction of tolerance in S3-specific B cells in mice primed with high doses of S3-RBC, and (b) induced differentiation of IgG-producing B cell precursors to Bgamma memory cells in mice primed with low doses of antigen.

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Secondary IgG responses to type 3 pneumococcal polysaccharide III. T cell requirement for development of B memory

Braley‐Mullen

1977

Eur J Immunol

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Split unresponsiveness to the trinitrophenyl determinant I. Manoeuvers which suppress either humoral or cell‐mediated immune responses

Ptak

Różycka

1977

Eur J Immunol

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2,4,6-Trinitrobenzene sulfonic acid (TNBS) injected intravenously (i.v.) makes mice fully tolerant to the trinitrophenyl (TNP) determinant. Administration of in vitro TNP-labeled syngeneic erythrocytes or thymocytes renders mice unable to develop contact sensitivity to picryl chloride, while the humoral anti-TNP responses seem to be unaffected. The reverse was found after pretreatment of mice with TNP-labeled isologous IgG (MGG) since only anti-TNP antibody responses, but not contact sensitivity to picryl chloride, were significantly reduced. TNP-coupled macrophages given to animals suppressed both the cell-mediated and humoral responses, and this might be due to the presence on their surface of TNP-labeled cytophilic antibody. TNBS administered i.v. binds to circulating proteins and formed blood elements. Thus the split unresponsiveness affecting either humoral or cell-mediated compartments after the injection of TNP-MGG or of haptenated cells respectively, is presumably due to dissecting events which in vivo after the injection of TNBS, occur simultaneously. These results may be interpreted to indicate that split unresponsive states to TNP determinants are mediated two independent mechanisms which require different tolerogen presentations to be triggered.

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Tolerance Induction and Maintenance in Primed Lymphocytes

Levich

Weigle

1985

Surv. immunol. Res.

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Preventive Effect of Hapten-Reactive Thymus-Derived Helper Lymphocytes on the Tolerance Induction in Hapten-Specific Precursors of Antibody-Forming Cells

Cited by 8 publications

References 0 publications

Secondary IgG responses to type 3 pneumococcal polysaccharide III. T cell requirement for development of B memory

Secondary IgG responses to type 3 pneumococcal polysaccharide III. T cell requirement for development of B memory

Split unresponsiveness to the trinitrophenyl determinant I. Manoeuvers which suppress either humoral or cell‐mediated immune responses

Tolerance Induction and Maintenance in Primed Lymphocytes

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