Antibodies against I-A and I-E determinants inhibit the activation and function of encephalitogenic T-lymphocyte lines

Halina Offner, Steven W. Brostoff, Arthur Vandenbark

Research output: Contribution to journalArticle

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Abstract

Two monoclonal antibodies, OX-6 and OX-17, were used to evaluate respectively the roles of I-A and I-E major histocompatibility complex Class II gene products in the in vitro activation and subsequent function in recipient rats of encephalitogenic T-cell lines. Activation of the T-cell lines with guinea pig myelin basic protein (GP-BP) presented by accessory cells (APC) resulted in an increase in the number of blast cells in culture and was reflected by increased uptake of [3H]thymidine ([3H]Tdy). The number of blasts recovered and [3H]Tdy uptake during activation was reduced drastically in the presence of OX-6, but to a much lesser extent in the presence of OX-17. OX-6 but not OX-17 appeared to block T-cell activation primarily by inhibiting APC function, since preincubation of APC but not T cells with OX-6 before stimulation resulted in complete inhibition of the cultures. After activation, the BP-1 T-cell line or D-9 clone transferred severe paralysis to normal recipient rats. Recipients of OX-6-treated BP-1 or D-9 T cells exhibited very mild or no signs, whereas recipients of OX-17-treated cells developed only slightly less severe experimental autoimmune encephalomyelitis (EAE) than recipients of untreated encephalitogenic control cultures. In contrast, treatment with OX-17 but not OX-6 reduced the ability of BP-reactive T cells to transfer delayed-type hypersensitivity reactions. Dermal testing with GP-BP in the ears of recipient rats just prior to onset of clinical signs decreased significantly the clinical intensity of EAE induced by activated BP-reactive T cells, but increased the clinical scores in rats which received unstimulated or OX-6-treated T cells. This potentiating effect of GP-BP was due most likely to the presentation of processed antigen to circulating BP-reactive T cells by APC in the ear. These results suggest that both the I-A and I-E gene products may contribute to the activation and subsequent function of encephalitogenic T cells, perhaps through separate mechanisms.

Original languageEnglish (US)
Pages (from-to)364-373
Number of pages10
JournalCellular Immunology
Volume100
Issue number2
DOIs
StatePublished - 1986

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T-Lymphocytes
Antibodies
Myelin Basic Protein
Guinea Pigs
Autoimmune Experimental Encephalomyelitis
Cell Line
Ear
MHC Class II Genes
Antigen Presentation
Delayed Hypersensitivity
Major Histocompatibility Complex
Paralysis
Thymidine
Clone Cells
Cell Culture Techniques
Skin
Genes

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

Antibodies against I-A and I-E determinants inhibit the activation and function of encephalitogenic T-lymphocyte lines. / Offner, Halina; Brostoff, Steven W.; Vandenbark, Arthur.

In: Cellular Immunology, Vol. 100, No. 2, 1986, p. 364-373.

Research output: Contribution to journalArticle

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