Monoclonal antibody against human T cell leukemia virus p19 defines a human thymic epithelial antigen acquired during ontogeny.

Abstract

Using monoclonal antibody 12/1-2 against a 19,000-dalton human T cell leukemia virus (HTLV) protein (anti-p19), previously demonstrated to be reactive with HTLV-infected human cells, but not in numerous other uninfected cells, we found a reactive antigen to be expressed on the neuroendocrine component of human thymic epithelial cells but not on any other normal epithelial or neuroendocrine human tissues. Moreover, this reactive antigen is acquired on neuroendocrine thymic epithelium during thymic ontogeny--first appearing on fetal thymic epithelial cells between 8 and 15 wk gestation. While only a portion of thymic epithelial cells in the subcapsular cortical region of 15- and 24-wk fetal thymuses contained anti-p19+ epithelial cells, the entire subcapsular cortical region of newborn thymus epithelium was anti-p19+. By age 3 yr, normal subjects' entire subcapsular cortical and medullary thymic epithelium was anti-p19+. Using antibody against HTLV core protein, p24, and c-DNA probes for HTLV DNA, neither HTLV-specific p24 protein nor proviral DNA could be demonstrated in anti-p19+ thymic epithelial tissue. However, thymic epithelial extracts, disrupted HTLV extracts, as well as purified HTLV p19 antigen all inhibited the binding of anti-p19 antibody to thymic epithelium. Thus, anti-p19 may recognize a determinant on an HTLV-encoded 19,000-dalton structural protein that is shared by human thymic epithelium. Alternatively, anti-p19 defines a host encoded protein that is selectively expressed by normal thymic epithelium, and is induced to be expressed in HTLV-infected malignant T cells.

HTLV‐1 in Switzerland: Low prevalence of specific antibodies in HIV risk groups, high prevalence of cross‐reactive antibodies in normal blood donors

“…In view of these epidemiologic conditions and also of the fact that neither screening of the normal blood donors by particle agglutination nor screening by ELISA resulted in any outright positives, the most likely interpretation of our results is the hypothesis that these weakly reactive antibodies are induced by one or several agents with some structural similarity to HTLV-I. These agents might be normal body proteins, since it has been shown that some MAbs to gag proteins of HTLV-l may also react with antigen of normal thymus (Haynes et al, 1983), or human placenta (Suni et al, 1984). However, it is more likely that the antibodies reacting to more than one of the final gag proteins might have been induced by an infectious agent, possibly a retrovirus distantly related to HTLV -1.…”

Immunoelectron microscopic localization of human T-cell leukemia virus type-I antigens.

“…The anti-p19 MoAb was shown to react with p19 in HUT 102, and with p19 and p28 in MT-2 as previously mentioned (40,41). Anti-p19 MoAbs from some clones were shown to react with, in addition to p19, normal thymic epithelial cells and some of the embryonal cells (7,27,38).…”

Human T Lymphotropic Virus Type I Associated Myelopathy and Myasthenia gravis: A Possible Association?

“…(3) The decre ment of the serum HTLV-I-Ab after thymectomy may, although tentative, raise the intriguing issue of a possible thymic involvement in regulating serum HTLV-I-Ab pro duction. (4) Although the iinmunohistological reaction of the thymic reticular cells may represent a cross-reaction of anti p i 9 antibody to a host protein as Haynes et al [17] reported, they also suggested that antigenicity induced in host T cells by HTLV-I infection may be coexpressed on normal thymic reticular cells. Existence in the present patient, and absence in the controls, of antigenicity for HTLV-I p 19 in thymic reticular cells might connote a pos sible involvement in HTLV-1 infection of thymic reticular cells, and, furthermore, of the interactions of these cells with thymocytes in the regulation of antibody production [ 18].…”