T Cell-Derived Antigen Binding Molecules (TABM): Molecular and Functional Properties

Cone, Robert E.; Zheng, Heguang; Chue, Ben; Beaman, Kenneth D.; Ferguson, T.; Green, Douglas R.

doi:10.3109/08830188809051189

Cited by 14 publications

(5 citation statements)

References 62 publications

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“…The regulatory activity from A1.1 participates in antigenspecific induction of suppression (4) and may be related to previously described T-cell suppressor-inducer factors (17)(18)(19). However, the factor from A1.1 is incomplete, requiring the "accessory supernatant" for function.…”

Section: Discussionmentioning

confidence: 55%

“…We have speculated previously that CD4' T cells, which bear a TCR with a sufficiently high affinity for antigen, may be directed into the suppressor pathway (by producing suppressor inducer molecules) upon exposure to antigen (5,17,28). Our results, reported herein, together with those of others discussed above, suggest that at least part of the resulting factor is intimately related to the TCR a molecule.…”

Section: Discussionmentioning

confidence: 99%

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Specific inhibition of cell-surface T-cell receptor expression by antisense oligodeoxynucleotides and its effect on the production of an antigen-specific regulatory T-cell factor.

Zheng

Sahai

Kilgannon

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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We have used antisense oligodeoxynucleotides corresponding to genes encoding the variable (V) region of the T-cell receptor (TCR) a and j3 chains (V. and Vp) to control TCR expression in T-cell hybridomas. Two hybridomas, A1.1 and B1.1, recognize a synthetic polypeptide antigen designated poly 18 {poly[Glu-Tyr-Lys-(Glu-Tyr-Ala)51} together with I-Ad. We have found that TCR function (production of lymphokines in response to antigen) and T3 expression were removed after protease treatment of the cells and were fully recovered 48 hr later. However, when antisense oligodeoxynucleotides corresponding to the appropriate TCR V genes were present after protease treatment, little or no recovery of TCR function or T3 expression was observed. This effect was specific for the TCR V genes utilized by the T cell: antisense oligodeoxynucleotides corresponding to the TCR V regions of AM.1 had no effect on TCR expression in B1.1 and vice versa. Thus, antisense oligodeoxynucleotides can be used to temporarily block expression of a TCR gene in a T-cell hybridoma. This technique was then applied to a paradoxical phenomenon in Al.1 cells. We had observed previously that Al.1 releases an antigen-specific immunoregulatory activity that shows the same antigenic fine specificity as is displayed by the TCR of AL.L. We now report that antisense oligodeoxynucleotides corresponding to the AM.1 V. gene blocked the production of this soluble antigen-specific activity by the cell. Antisense oligodeoxynucleotides corresponding to All Vp, on the other hand, had no effect on the production of this antigen-specific activity. We discuss these observations in the context of recent findings on the nature of T cell-derived antigen-specific regulatory factors.T lymphocytes specifically recognize foreign antigen together with self major histocompatibility complex (MHC) molecules through the cell-surface T-cell receptor (TCR) complex. This complex is composed of the TCR a and p chains, which are responsible for antigen and MHC specificity (1), and the T3 molecules, which may be responsible for transducing the membrane signal (2). a Chain, p chain, and T3 are only expressed as a complex; in the absence ofany one component, cell-surface expression does not occur (2).A helper T-cell hybridoma (A1.1) has been described (3) that expresses TCR a and 8 molecules specific for a synthetic polypeptide designated poly 18 {poly[Glu-Tyr-Lys-(Glu-TyrAla)5]} and, in the presence of specific antigen and I-Ad, releases lymphokines. This T-cell hybridoma also constitutively produces a poly 18-specific cell-free factor involved in antigen-specific induction of suppression, which we call "suppressor-inducer factor" (4). Analysis has revealed (4) that the factor produced by Al. 1 displayed the same antigenic fine specificity exhibited by the TCR on the Al.1 cell surface.Further, an anti-TCR antiserum was found to bind the antigen-specific factor (5). These results led us to speculate that at least some of the genes encoding the TCR a and 83 chains may be responsibl...

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Specific inhibition of cell-surface T-cell receptor expression by antisense oligodeoxynucleotides and its effect on the production of an antigen-specific regulatory T-cell factor.

Zheng

Sahai

Kilgannon

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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“…The TABM isolated from this patient seems to be a distinct protein, because AF does not bind to type I collagen (10). TABM have been reported to produce diverse immunoregulatory (36) and inflammatory (12) effects, suggesting that production of the 60-kd type I collagen-binding protein plays a role in the pathogenesis of this patient's highly unusual connective tissue disease.…”

Section: Discussionmentioning

confidence: 99%

“…36). The antigen-binding capacity distinguishes this protein from conventional interleukins, which do not bind to this type I collagen preparation (10,ll).…”

Section: Discussionmentioning

confidence: 99%

“…The T cell origin and the ability to bind nominal antigen, i.e., type I collagen, suggest that the lymphokine is a human analog of a class of mouse proteins termed T cell-derived antigen-binding molecules (TABM) (for review, see ref. 36). The antigen-binding capacity distinguishes this protein from conventional interleukins, which do not bind to this type I collagen preparation (10,ll).…”

Section: Discussionmentioning

confidence: 99%

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Intractable vasculitis, resorptive osteolysis, and immunity to type i collagen in type viii ehlers‐danlos syndrome

Hoffman

Filie

Schumacher

et al. 1991

Arthritis & Rheumatism

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A unique patient with type VIII Ehlers‐Danlos syndrome and cutaneous vasculitis, resorptive osteolysis, and cardiac valvular disease is described. Collagen analyses identified morphologic and physical abnormalities of type I collagen. The patient's T lymphocytes could be propagated in vitro with type I collagen and produced a 60‐kd lymphokine that bound this protein. Cellular autoimmunity to type I collagen may be responsible for this patient's intractable clinical condition.

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Influence of the Anterior Chamber of The Eye on T-Cell Production of Extracellular Antigen-Specific Proteins

Cone

Hadjikouti

Wang

et al. 1995

Advances in Experimental Medicine and Biology

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T Cell-Derived Antigen Binding Molecules (TABM): Molecular and Functional Properties

Cited by 14 publications

References 62 publications

Specific inhibition of cell-surface T-cell receptor expression by antisense oligodeoxynucleotides and its effect on the production of an antigen-specific regulatory T-cell factor.

Specific inhibition of cell-surface T-cell receptor expression by antisense oligodeoxynucleotides and its effect on the production of an antigen-specific regulatory T-cell factor.

Intractable vasculitis, resorptive osteolysis, and immunity to type i collagen in type viii ehlers‐danlos syndrome

Influence of the Anterior Chamber of The Eye on T-Cell Production of Extracellular Antigen-Specific Proteins

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