Biomedical subjects

S L Tiegs

Publications and source records attributed to S L Tiegs.

3 recordsLinked to original sources

PubMed1993

Receptor editing in self-reactive bone marrow B cells.

A central paradigm of immunology is clonal selection: lymphocytes displaying clonally distributed antigen receptors are generated and subsequently selected by antigen for growth or elimination. Here we show that in mice transgenic for anti-H-2Kk,b antibody genes, in which a homogeneous clone of developing B cells can be analyzed for the outcome of autoantigen encounter, surface immunoglobulin M+/idiotype+ immature B cells binding to self-antigens in the bone marrow are induced to alter the specificity of their antigen receptors. Transgenic bone marrow B cells encountering membrane-bound Kb or Kk proteins modify their receptors by expressing the V(D)J recombinase activator genes and assembling endogenously encoded immunoglobulin light chain variable genes. This (auto)antigen-directed change in the specificity of newly generated lymphocytes is termed receptor editing.

Animals↗

PubMed1990

Delayed antigen presentation by epidermal Langerhans cells to cloned T h1 and T h2 cells.

Langerhans (LC) cells require incubation with protein antigen for several days before the cells effectively stimulate proliferation of cloned, H-2 restricted, antigen-specific T h cells. In contrast, splenic antigen-presenting cells are immediately effective. LC are immediately competent, however, if an immunogenic peptide rather than the intact protein is the immunogen, indicating that resident or unchallenged LC have the required class II MHC and can provide the signals necessary for T-cell proliferation but may lack the capacity to internalize or cleave protein antigens. We propose that delayed antigen presentation by LC may be intrinsic and advantageous for promoting early systemic immunity. LC stimulate cloned T h1 and T h2 cells equally well, suggesting that LC may not limit or bias the type of immunity that occurs with cutaneous antigenic challenge.

Animals↗

PubMed1987

Transforming growth factor-beta: selective increase in glycosaminoglycan synthesis by cultures of fibroblasts from patients with progressive systemic sclerosis.

Transforming growth factor-beta (TGF-beta) has been found in all cells examined thus far, and has been shown to play an important role in inflammation and connective tissue formation. We now report that TGF-beta, alone or in combination with epidermal growth factor (EGF), led to a preferential increase in glycosaminoglycan synthesis by cultures of dermal fibroblasts from patients with progressive systemic sclerosis (PSS) when compared with normal fibroblasts (p less than 0.001). Transforming growth factor-beta increased collagen synthesis to the same extent in both PSS and normal fibroblasts, whereas EGF had no stimulatory activity on collagen synthesis. The addition of EGF to cultures incubated with TGF-beta led to a decrease in collagen synthesis compared with the effect seen with TGF-beta alone (p less than 0.02). These studies suggest that TGF-beta may play an important role in the accumulation of connective tissue seen in PSS and that the combined action of multiple growth factors may modulate the synthetic activity of human dermal fibroblasts.

Cells, Cultured↗