In this review we discuss the results of studies about the effect of stress, depression, anxiety, social support and various psychosocial treatments on numbers and activity of Natural Killer (NK) cells. In general a suppressive effect is observed among depressive persons and persons who react to stressfull events with feelings of helplessness and anxiety. Lack of social support also seems to engender immunosuppression including NK suppression. Various forms of psychosocial care seem to be able to undo these negative consequences. However, the real clinical relevance of these findings is still a matter of dispute.

Indicator traits used to select pigs for increased resistance to infection or improved health must be heritable and, preferably, be associated with improved performance. We estimated the heritability of a range of immune traits and their genetic and phenotypic correlations with growth performance. We measured immune traits on 589 pigs and performance on 1941 pigs from six farms, three of which were classified as ‘high health status’ (i.e. specific pathogen-free) and three were of lower health status. All pigs were apparently healthy. Immune traits were total white blood cells (WBC), and peripheral blood mononuclear leucocyte (PBML) subsets positive for CD4, CD8α, gamma delta (γδ) T cell receptor, CD11R1 (natural killer cell marker), B cell and monocyte markers at the start and the end of standard growth performance tests. At both time points, all immune traits were moderately to highly heritable except for CD8α+ cells. At end of test, heritability estimates (h2) (±s.e.) were 0.18 (±0.11) for total WBC count. For PBML subset proportions, the heritabilities were 0.52 (±0.14) for γδ TCR+ cells, 0.62 (±0.14) for CD4+ cells, 0.44 (±0.14) for CD11R1+ cells, 0.58 (±0.14) for B cells and 0.59 (±0.14) for monocytes. Farm health status affected the heritabilities for WBC, being substantially higher on lower health status farms, but did not have consistent effects on heritabilities for the PBML subsets. There were significant negative genetic correlations between numbers and proportions of various PBML subsets and performance, at both start and end of test. In particular, the proportion of PBML cells that were CD11R1+ cells, at end of test, was strongly correlated with daily gain (rg = −0.72; P < 0.01). There were also weaker but significant negative phenotypic correlations between PBML subsets measured at end of test and performance, for γδ+ T cells, CD8α+, CD11R1+ cells, B cells or monocytes. Phenotypic correlations with daily gain were generally lower at the start of test than at the end of test. These results show that most of the major pig PBML subsets are heritable, and that systemic levels of several of these PBML subsets are genetically negatively correlated with performance. This approach provides a basis for using immune trait markers when selecting boars that can produce higher-performing progeny.

The process of wound healing begins with an inflammatory reaction that is principally dependent on cellular immune elements. Although the involvement in wound healing of leucocytes that mediate nonspecific immunity (e.g. neutrophils and macrophages) is well known, the participation of cells which prime the immune reaction, i.e. the lymphocytes, requires further investigation. This study was performed to examine the temporal sequence and kinetics of these cells during cutaneous wound repair. The model selected was a full-thickness skin excisional wound made on the flanks of female Wistar rats. At time points ranging from 3 h to 2 wk wound samples were processed for polyester wax-embedding. Target antigens were identified and monitored quantitatively in sections stained immunohistochemically. Monoclonal antibodies against neutrophils, macrophages, pan T cells and cytotoxic populations of lymphocytes were used. The results showed that these cells are involved in the process of wound healing in a distinctive dynamic pattern. The accumulation of CD3+ T lymphocytes in the wound bed was mainly associated with the phase of granulation tissue formation. Intraepithelial CD3+ T lymphocytes were detected in considerable numbers within the regenerating epidermis. The cytotoxic cell populations (OX8+ ) were classified morphologically into the cytotoxic/suppressor subset of T cells and NK cells. The OX8+ T cells were shown to have a kinetic pattern similar to CD3+ T lymphocytes but of a lower magnitude. The accumulation of OX8+ NK cells was confined to the early inflammatory phase of repair. It is concluded that CD3+ T lymphocytes as well as OX8+ cytotoxic populations of the immune system are involved in the process of cutaneous wound healing in temporal sequences which suggest that they may be involved in its modulation.

Breast cancer is a complex disease. Its aetiology is multifactorial, its period of development can span decades, and its clinical course is highly variable. Evaluation of the role of the immune response in either the development or control of breast cancer is also complex. Nevertheless, there is substantial information that in this disease, the immune response is not a host defence reaction and may even serve to facilitate cancer development. This evidence comes from a variety of sources including clinical–pathological investigations in women that show a correlation between the intensity of lymphocytic infiltration into the tumour mass with poor prognosis, studies in breast cancer patients that demonstrate a similar correlation between delayed hypersensitivity reactivity or in vitro assays of immune reactivity to tumour cell membranes or non-specific antigens and poor prognosis, and analyses of cancer incidence in chronically immunosuppressed, kidney transplant recipients who develop an unexpectedly low incidence of breast cancer. The overall conclusions from these human studies are corroborated by observations in mouse mammary tumour models that also demonstrate immune enhancement of breast cell proliferation in vitro and of breast cancer development in vivo. Potential mechanisms for these effects include production, by inflammatory cell infiltrates, of direct or indirect modulators of breast cell growth, e.g. cytokines, peptide or steroid hormones, enzymes involved in steroid metabolism, as well as of antibodies to growth factors or their receptors. These immune facilitatory mechanisms must be overcome if immune-based therapies are to be applied successfully in breast cancer.