The allele frequency net database (http://www.allelefrequencies.net) is an online repository that contains information on the frequencies of immune genes and their corresponding alleles in different populations. The extensive variability observed in genes and alleles related to the immune system response and its significance in transplantation, disease association studies and diversity in populations led to the development of this electronic resource. At present, the system contains data from 1133 populations in 608 813 individuals on the frequency of genes from different polymorphic regions such as human leukocyte antigens, killer-cell immunoglobulin-like receptors, major histocompatibility complex Class I chain-related genes and a number of cytokine gene polymorphisms. The project was designed to create a central source for the storage of frequency data and provide individuals with a set of bioinformatics tools to analyze the occurrence of these variants in worldwide populations. The resource has been used in a wide variety of contexts, including clinical applications (histocompatibility, immunology, epidemiology and pharmacogenetics) and population genetics. Demographic information, frequency data and searching tools can be freely accessed through the website.

We identified a novel phenotype of SF NK cells that is of potential significance in RA. Experiments are now under way to determine the function of these SF NK cells and their potential role in RA.

Human T cells expressing CD56 are capable of tumour cell lysis following activation with interleukin-2 but their role in viral immunity has been less well studied. Proportions of CD56(+) T cells were found to be highly significantly increased in cytomegalovirus-seropositive (CMV(+) ) compared with seronegative (CMV(-) ) healthy subjects (9.1 ± 1.5% versus 3.7 ± 1.0%; P < 0.0001). Proportions of CD56(+) T cells expressing CD28, CD62L, CD127, CD161 and CCR7 were significantly lower in CMV(+) than CMV(-) subjects but those expressing CD4, CD8, CD45RO, CD57, CD58, CD94 and NKG2C were significantly increased (P < 0.05), some having the phenotype of T effector memory cells. Levels of pro-inflammatory cytokines and CD107a were significantly higher in CD56(+) T cells from CMV(+) than CMV(-) subjects following stimulation with CMV antigens. This also resulted in higher levels of proliferation in CD56(+) T cells from CMV(+) than CMV(-) subjects. Using Class I HLA pentamers, it was found that CD56(+) T cells from CMV(+) subjects contained similar proportions of antigen-specific CD8(+) T cells to CD56(-) T cells in donors of several different HLA types. These differences may reflect the expansion and enhanced functional activity of CMV-specific CD56(+) memory T cells. In view of the link between CD56 expression and T-cell cytotoxic function, this strongly implicates CD56(+) T cells as being an important component of the cytotoxic T-cell response to CMV in healthy carriers.

No abstract