Small intestine intraepithelial lymphocytes (IELs) comprise a heterogeneous and phenotypically complex population of T cells that are part of the gut-associated lymphoid tissues (GALTs). Recent studies from a number of laboratories indicate that murine IELs are greatly enriched for extrathymic T cells, although many aspects of the IEL+ extrathymic developmental pathway remain controversial, and there is currently no consensus of opinion as to which IELs are extrathymic and which are thymus-derived. Those differences reflect variations in the IEL repertoire in athymic animals depending upon the specific model used to study IELs, and they correlate with the age at which mice became or were rendered athymic, implying that the thymus participates either directly or indirectly in the local extrathymic IEL developmental process. In this article, the basic findings regarding intestinal T cell development are discussed, and a hypothesis is provided which links neuroendocrine interactions targeted to the intestine epithelium to the striking relationship between animal developmental age and the thymopoietic potential of the intestine.
Schistosomiasis is a parasitic disease in which focal inflammatory responses called granulomas develop in the liver and intestines. The inflammatory cells within these granulomas produce authentic vasoactive intestine peptide (VIP). VIP acts as an immune modulator. In the schistosome granuloma, VIP can suppress T cell proliferation and T lymphocyte IL-2 production. Also, it can enhance IL-5 production from granuloma T cells. The granuloma T cells bear authentic VIP receptors of both the VIPr1 and VIPr2 subclasses. It is probable that the expression of these receptors is subject to immunoregulation, which is the topic of current investigation. Moreover, differences in the structure of VIPr1 and VIPr2 suggest that each may have unique immunoregulatory functions in inflammation.
The aim of this clinical review is to highlight recent advances in immunology, as well as new information from selected other areas, which have led to a better appreciation of the neuroimmunologic mechanisms involved in Multiple sclerosis (MS). New data on immunopathology, the cytokine network, and the role of oligodendrocytes, lymphocytes, and endothelial cells in this disease, have produced novel therapeutic approaches. New information on clinical course and neuroimaging disease features, as well as the role of genetic factors and infectious agents, have also improved our understanding of the immune basis for MS.
The belief that cancer might be related to temperament or distress has been emphasized throughout the history of medicine. The field of psychoneuroimmunology has its origins in psychosomatic medicine, and has evolved to the investigations of complex interactions between the psyche and the nervous, immune, and endocrine systems. Such interactions may have implications in both cancer risk and survival.
Our previous studies have shown that prolactin (PRL), a pituitary and lymphocyte hormone and a ligand of the cytokine/hemopoietin receptors (R) superfamily, acts synergistically with interleukin (IL)-2 on the development of lymphokine activated killer (LAK) cells and enhances the effects of GM-CSF and IL-3 on myeloid progenitors' proliferation and differentiation. More recently, we have demonstrated that GM-CSF and IL-3 increase the sensitivity of acute myeloid leukemic (AML) cells to LAK activity. Together, these findings have prompted us to study the role of PRL on the target arm of the LAK response. We show here that CD33+ blasts from AML patients express membrane PRL-R and that the PRL/PRL-R interaction is followed by increased susceptibility to natural killer (NK) (p < 0.02) and LAK (p < 0.001) cells. As predicted from the dimerization model of PRL-R and in agreement with previous reports, the response of AML blasts to PRL was bell-shaped with a trend peak at 25 ng/ml. Although enhanced lysis occurred at the target recognition level, it was not accompanied by changes in the MHC class I, cellular adhesion molecules, or myeloid differentiation antigens. Cell cycle recruitment and lysis increased concurrently in three cases studied, suggesting a modulatory action of PRL on the expression of putative cycle-related NK/LAK-target structures. Together, these data strengthen the role of PRL in the LAK response.
