A D Duby

Detection of a frequent restriction fragment length polymorphism in the human T cell antigen receptor beta chain locus. A potential diagnostic tool.

Abnormal T cell function is a feature of a spectrum of inherited and acquired diseases. We have detected a frequent restriction fragment length polymorphism in the human T cell antigen receptor beta-chain locus that may aid in the analysis of these disorders. A study of a panel of 18 normal individuals, testing for the presence of the polymorphism, showed it to account for 36% of the alleles in that group. In view of the fact that the T cell receptor beta-chain locus has been mapped to chromosome 7, and that the disease ataxia telangiectasia (AT) is associated both with abnormal T cell function and with chromosomal abnormalities of the same region of chromosome 7, we investigated the possibility that the polymorphism could demonstrate linkage of the T cell receptor locus to the gene for that disease. We demonstrated that the mutation causing AT did not lie within the beta-chain locus itself, and that there was preliminary evidence that the two loci were not closely linked. This polymorphism may provide a useful tool for the study of other genetic disorders associated with abnormalities of T cell function, as well as disorders associated with inherited or acquired abnormalities of chromosome 7.

An Ia-positive mouse T-cell clone is functional in presenting antigen to other T cells

In this report we present data demonstrating the endogenous expression of I-region associated (la) antigens on a cloned line of mouse T cells, CTLL, as well as transcription of the invariant chain gene in these cells. We demonstrate further that this Ia-bearing T-cell clone, CTLL, can utilize the expressed la molecules to present antigen to la-restricted antigen-specific T cells.

Sequestration of virus-specific T cells in the cerebrospinal fluid of a patient with varicella zoster viral meningoencephalitis

The frequency of virus-specific T cells in the cerebrospinal fluid of a patient with viral infection of the brain and meninges was determined by using a single-T-cell cloning technique where a representative sampling of T cells was cloned from the cerebrospinal fluid of a patient with varicella zoster viral (VZV) meningoencephalitis. That the derived T-cell clones were in fact clonal was shown by demonstrating, on Southern blot analyses, unique rearrangements of the T-cell antigen-receptor beta-chain genes of each clone. Five out of the 15 of the T4+ (CD4), 0/4 of the T8+ (CD8), and 0/1 of the T4+T8+ T-cell clones proliferated to VZV, while no clones proliferated to mumps virus or myelin basic protein. There was no clonal expansion of any VZV-reactive T cell in this patients cerebrospinal fluid. As VZV meningoencephalitis is thought to be due to the reactivation of a dormant herpes zoster viral infection, it can be regarded as a secondary immune response. The presence of different T-cell receptor beta-chain gene rearrangements in each T-cell clone suggests that the T-cell response was polyclonal. These results demonstrate that a high frequency of polyclonal, T4+ antigen-specific T cells can be found in a naturally occurring, localized, immune response.