Changes in the galactose content of IgG during humoral immune responses.

The Fc region of IgG bears two oligosaccharides of variable composition. The serum level of one variant which lacks terminal galactose and sialic acid (agalactosyl IgG) is raised in a number of autoimmune diseases and animal models thereof. Here it is shown that such changes in IgG glycosylation occur during non-pathological humoral immune responses. It was found that if specific pathogen free (SPF) CBA/Ca mice are transferred from a sterile to a conventional environment, their levels of total serum IgG rise whereas the degree of IgG galactosylation falls. Next, mice were immunised with bovine serum albumin (BSA) in incomplete Freund's adjuvant. As anti-BSA titres rose the antibodies became less galactosylated and later, as the titres fell, the antibodies became more galactosylated. By contrast, there was little or no variation in the relative galactosylation of total IgG. It is considered that the galactosylation of IgG antibodies varies during an immune response.

In vitro genetically aberrant T-cell clones with continuous growth are associated with atopic dermatitis.

Atopic dermatitis is a disease with a genetic predisposition affecting the immune system, with T lymphocytes participating in the immune dysregulation. Most in vitro T lymphocyte studies of atopic dermatitis have focused on antigen-specific T-cell clones. However, antigen-non-specific regulatory T lymphocytes may also take part in the pathway leading to antigen-specific clonal T-lymphocyte proliferation. T lymphocytes from skin biopsy specimens from three patients with severe atopic dermatitis were cultured in the presence of IL-2 and IL-4, but without antigen added. Initially, proliferation was oligo- or polyclonal, but in all cases overgrowth by T cells with clonal chromosomal aberrations was subsequently observed. These abnormal T-cell clones demonstrated continuous growth and complete or partial phenotypic loss of the T-cell antigen receptor complex. In summary, these findings suggest that a subset of aberrant skin-homing T lymphocytes is associated with atopic dermatitis.