Serum levels of interleukin‐10 (IL‐10) are elevated in a proportion of patients with untreated chronic hepatitis C, and this may compromise the host immune response to the virus. The capacity for IL‐10 production varies according to the genetic composition of the IL‐10 locus. We examined the inheritance of 3 biallelic polymorphisms in the IL‐10 gene promoter in patients with chronic hepatitis C and their association with response to treatment with interferon alfa (IFN‐α). After adjusting for potential confounding variables, a highly significant relationship was found between inheritance of the IL‐10 promoter −592*A and −819*T alleles or the ATA haplotype and response to IFN‐α therapy (P = .016). Response to treatment was also associated with viral genotype 3a, a low viral load, and less fibrosis on liver biopsy. Following in vitro stimulation of peripheral blood mononuclear cells, the IL‐10 promoter haplotypes, GCC, ACC, and ATA, were associated with high, intermediate, and low IL‐10 production, respectively. These findings indicate that heterogeneity in the promoter region of the IL‐10 gene has a role in determining the initial response of chronic hepatitis C to IFN‐α therapy. Patients who are genetically predisposed to high IL‐10 production have a poor response to IFN‐α and may benefit from additional treatment strategies designed to enhance a T‐helper type 1 (Th1) response.

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The elevated levels of MCP-1, IL-6, and IL-8 in peritoneal fluid but not serum may indicate the importance of local macrophage activating factors in the pathogenesis of endometriosis.

While raised cellular immunity mediated by T helper (Th) 1 type cells may be harmful for the developing embryo/foetus, it is likely that Th2 type immunity may be helpful. The role of natural killer (NK) cells is presently underestimated, although they are clearly important in angiogenesis and the coordinated invasion of the decidua by the trophoblast. Deficient T regulatory cell (Treg) function is evident in women with recurrent miscarriage particularly when this occurs in early pregnancy. The role of the pro-inflammatory Th17 cells is presently unclear. However, early evidence suggests that excessive Th17 activity may promote miscarriage and preterm delivery. This may relate to the ability of these cells to produce those cytokines that encourage Th1 and NK cell activity. As such recurrent miscarriage may be caused not only by chromosomal abnormalities, autoimmunity and uterine abnormalities but also by subclinical uterine infection and inflammation which by stimulating interleukin 6 favours Th17 development over Tregs. This review examines the role of these different cells in early pregnancy and suggests a schema that may join the dots of the immunological puzzle called pregnancy. Finally, suggestions are made as to how inappropriate immunity in recurrent miscarriage may be down-regulated using currently available therapies.