III Antibodies A Monoclonal antibodies against determinants of the HLA-A,-B,-C glycoproteins and pjmicroglobulin 1. Antibodies against species specific, non-polymorphic determinants 2. Antibodies against polymorphic HLA-A,-B,-C determinants B Monoclonal antibodies against HLA-DRw determinants 1. Antibody against a species specific HLA-DRw determinants 2. Antibodies against polymorphic HLA-DRw determinants

Citation-classic - monoclonal-antibodies for analysis of the hla system

Articles in the recent literature document an abnormal antibody response in elderly persons to influenza vaccination. Several studies have presented evidence to show that immune dysfunction in aged mice and humans may be due to a defect in the production of interleukin 2 (IL2) by helper T cells (TH). Cultures of peripheral blood mononuclear cells (PBMC) were prepared from blood samples taken at eight weeks after vaccination (0.5 mL of Armand-Frappier, 15 micrograms/0.5 mL each of A/Taiwan/1/86, A/Leningrad/360/86, and B/Ann Arbor/1/86 administered in the fall of 1987) from a group of elderly men and a young control group. Peripheral blood mononuclear cells were frozen in 10% dimethyl sulfoxide (DMSO) until all the cells were cultured. After stimulation with a 1/320 dilution of the same influenza vaccine, cultures of PBMC from young controls showed a significantly greater increase in IL2 production than the cultures of PBMC from the elderly group of patients. This was statistically significant at both day 3 (P less than .01) and day 5 (P less than .05) of culture using the Mann-Whitney U test. Previous experiments that have shown defective IL2 production related to aging have used potent mitogens such as concanavalin A and phytohemagglutinin to stimulate TH. This study provides evidence that defective IL2 production may also occur in response to physiologic antigenic stimulation and may be one explanation for the reduced efficacy of influenza vaccination in elderly persons.

Age-related decline in interleukin 2 production in response to influenza vaccine.

Over the past 20 years, it has become increasingly clear that thymus-derived lymphocytes (T lymphocytes) play a pivotal role in immune responsiveness. Perhaps nowhere is this more apparent than in antiviral immunity, in which T lymphocytes provide a critical helper function in antibody responses and also function directly to reduce viral replication. Of the large number of viruses known to elicit T-lymphocyte responses, influenza virus has been the most extensively studied.

Specificity and Function of T Lymphocytes Induced by Influenza A Viruses

Human T cell clones specific for tetanus toxoid (TT) or for alloantigens were isolated and expanded in culture using antigen stimulation and soluble growth factors. When stimulated by the specific antigen, the clones were able to proliferate in the absence of exogenous growth factors and to provide help to B cells. The alloreactive and TT-specific clones were compared for their capacity to help an anti-TT as well as a polyclonal antibody response. The frequency of the B cells activated to the production of specific antibody was determined by limiting dilution analysis in cultures containing limiting numbers of responding B cells and optimal numbers of cloned T helper cells. In these conditions a single activated B cell was able to produce about 10 ng of antibody. TT-specific clones, in the presence of low TT concentrations, selectively induced a number of TT-specific B cells to produce IgG antibody in the absence of a detectable polyclonal B cell activation. On the other hand the alloreactive clones activated higher numbers of TT-specific B cells as a part of a strong polyspecific B cell activation. In this case the antibody production did not require the presence of TT in culture; furthermore cells producing antibodies of unrelated specificities were also activated in allostimulated cultures. IgG anti-TT were produced only by immune donors, while IgM anti-TT were produced by immune and nonimmune donors, providing the B cells were activated by alloreactive clones.

These data demonstrate that human memory B cells can be triggered by both antigenspecific and alloreactive T cells to antibody production. The alloreactive clones can therefore be used to analyze at the clonal level the repertoire of a pool of B cells that contain most, if not all, the memory antibody specificities.

Activation of human B lymphocytes: frequency of antigen-specific B cells triggered by alloreactive or by antigen-specific T cell clones

Humoral and cell-mediated immunity to vero cell-derived influenza vaccine.

A human helper T cell line (F14m) activated by the matrix protein purified from A/X31 influenza virus has been developed After activation by antigen for 7 days, and reculture with matrix protein and irradiated autologous feeder cells, the cells obtained from an in vivo influenza virus-immunized donor have been growing in the presence of interleukin 2 for more than 7 months The cells all belong to the helper-inducer T cell subset and most of them express surface membrane HLA-DR antigens A small number (approximately 10(3)) of F14m T cells provided optimal help for 1 X 10(5) autologous T-depleted lymphocytes for production of anti-A/X31 but not anti-B/HK antibodies The F14m T cells produce soluble factors (S14m) able to help B cells to secrete anti-A/X31 antibodies F14m and S14m were shown to help antibody production to hemagglutinin when cultured with B cells and the whole virus The specificity of the T cell line for type-A matrix protein was confirmed by the ability of S14m to provide help for anti-A/JAP (A/H2/N2) but not for anti-B/HK antibody production These data provide evidence for matrix protein-specific T helper cells and factors able to provide help for antibody production against hemagglutinin, a distinct protein of the same virus

An influenza virus matrix protein‐specific human T cell line with helper activity for in vitro anti‐hemagglutinin antibody production

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An influenza virus matrix protein‐specific human T cell line with helper activity for in vitro anti‐hemagglutinin antibody production