DreamPharm Products:
Int Immunopharmacol. 2002 Sep;2(10):1477-89.
Immune stimulation in urethane-exposed pregnant mice increases expression level of spleen leukocyte genes for TGFbeta3 GM-CSF and other cytokines that may play a role in reduced chemical-induced birth defects.
Sharova LV, Gogal RM Jr, Sharov AA, Chrisman MV, Holladay SD.
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg 24061-0442, USA.
For unknown reasons, activation of the maternal immune system in mice reduces morphologic defects caused by diverse teratogenic agents. Such immune stimulation of the maternal animal has been correlated with altered cytokine mRNA transcripts in the placenta (e.g., TGFbeta2) as well as in fetal target tissues of the teratogen (e.g., TNFalpha in fetal heads of cyclophosphamide-exposed pregnant mice). The teratogen urethane was reported to down-regulate cell cycle and apoptotic regulatory genes in fetal mouse heads that displayed cleft palate, an effect that was also reversed by maternal immune stimulation. The molecular mediators of the above phenomena have not been identified, however proteins synthesized and released by activated maternal immune cells have been suggested. The present studies therefore evaluated the effects of maternal immune stimulation in urethane-exposed mice on thymus and spleen leukocyte populations, in an attempt to identify events that may correlate with protection against birth defects. Immune stimulation did not change the hypocellularity of the thymus nor the altered T cell differentiation caused by urethane. A limited and transient increase in splenic leukocyte number, including increased T and B lymphocytes and macrophages, was caused by immune stimulation and was not felt to play a significant role in reduced morphologic defects. Urethane treatment caused down-regulated expression of numerous genes involved in cell-cycle control, while maternal immune stimulation caused comparative up-regulation of many of these genes. Coordinate shifts in gene expression by treatment were evaluated using principal component analysis, which identified several growth factor genes that were differentially expressed in mice receiving urethane alone as compared to urethane plus immune stimulation. Up-regulated expression of TGFbeta3 and GM-CSF genes, in particular, was observed in leukocytes of urethane-exposed mice receiving immunostimulation. Interestingly, the cytokine products of these two genes were recently suggested as growth factors that may be related to reduction of fetal defects caused by teratogens. Genes for growth factors IGF-I, IGF-II and IL-2 were also identified as differentially expressed in urethane vs. urethane+immune stimulation mice, suggesting that these proteins should be considered for a potential contributing effect to reduced birth defects caused by immunostimulation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12400877&dopt=Abstract
Int Immunopharmacol. 2002 Sep;2(10):1495-501.
Effects of dietary wheat germ deprivation on the immune system in Wistar rats: a pilot study.
Chignola R, Rizzi C, Vincenzi S, Cestari T, Brutti N, Riviera AP, Sartoris S, Peruffo AD, Andrighetto G.
Dipartimento Scientifico e Tecnologico, Universita di Verona, Italy. chignolci.univr.it
Bioactive molecules that can gain access to body tissues through the gastrointestinal tract may interact with immune regulatory circuits and effector functions. Among these are plant lectins, such as wheat germ (WG) agglutinin, which constitute common components of the human diet and target the immune system on a daily basis. Dietary bioactive molecules might be considered as immunomodulatory signals. To investigate the possible effects on the immune system of the long-term absence of such signals, two groups of rats were fed on a diet containing or deprived of WG. The WG-deprived diet induced a state of functional unresponsiveness in lymphocytes from primary and secondary lymphoid organs, as evaluated by in vitro stimulation with T cell mitogen phytohemoagglutinin (PHA) and B cell mitogen lypopolysaccarides (LPS). The unresponsive state of the immune cells could be reversed by injection of antigen emulsified in oil with inactivated mycobacteria (complete Freund's adjuvant, CFA) Dietary signals can thus interact with the immune system possibly influencing its shaping during ontogenesis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12400879&dopt=Abstract
Trends Immunol. 2002 Nov;23(11):530-4.
Autoimmunity on alert: naturally occurring regulatory CD4(+)CD25(+) T cells as part of the evolutionary compromise between a 'need' and a 'risk'.
Schwartz M, Kipnis J.
Dept of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel. michal.schwarteizmann.ac.il
Autoimmunity, at least in the central nervous system (CNS), is not only an outcome of immune system malfunction, but is the body's own protective mechanism against destructive self-compounds. Likewise, the naturally occurring regulatory CD4(+)CD25(+) T cells have a physiological function, and are not merely an evolutionary adaptation to suppress self-reactive T-cell clones that escaped deletion in the thymus. We postulate that the regulatory T (Tr) cells are the product of an evolutionary compromise between the need for autoimmunity on alert for tissue maintenance and the need to control autoimmunity to avoid autoimmune disease. In the event of an insult to the CNS, the balance between self-reactive (effector) T cells and Tr cells determines the time of onset, the intensity and the duration of the autoimmune response. This response might thus represent an adaptive mechanism, which is optimal for day-to-day maintenance, but insufficient in extreme cases of CNS damage or failure of regulation. Downregulation or upregulation of CD4(+)CD25(+) Tr cells might be a way to achieve better protection from neurodegenerative conditions induced by self-destruction or avoid autoimmune inflammatory disease development, respectively.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401405&dopt=Abstract
J Exp Med. 2002 Dec 16;196(12):1575-84.
CD1-mediated gamma/delta T cell maturation of dendritic cells.
Leslie DS, Vincent MS, Spada FM, Das H, Sugita M, Morita CT, Brenner MB.
Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital at Harvard Medical School, Boston, MA 02115, USA.
Immature myeloid dendritic cells (DCs) express only low levels of major histocompatibility complex (MHC) class II but express high levels of CD1 a, b, and c antigen-presenting molecules at the cell surface. As Vdelta1+ gamma/delta T cells are the main tissue subset of gamma/delta T cells and they are known to recognize CD1c in the absence of specific foreign antigen recognition, we examined the possible interaction of these T cells with immature DCs. We show that CD1-restricted gamma/delta T cells can mediate the maturation of DCs. DC maturation required cell-cell contact and could be blocked by antibodies against CD1c. The maturation process was partially mediated by tumor necrosis factor alpha. Importantly, immature DCs matured in the presence of lipopolysaccharide and CD1-restricted gamma/delta T cells produced bioactive interleukin-12p70. In addition, these DCs were able to efficiently present peptide antigens to naive CD4+ T cells. CD1-restricted gamma/delta T cell recognition of immature DCs provides the human immune system with the capacity to rapidly generate a pool of mature DCs early during microbial invasion. This may be an important source of critical host signals for T helper type 1 polarization of antigen-specific naive T cells and the subsequent adaptive immune response.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12486100&dopt=Abstract
Diabetes. 2002 Nov;51(11):3254-62.
The iddm4 locus segregates with diabetes susceptibility in congenic WF.iddm4 rats.
Mordes JP, Leif J, Novak S, DeScipio C, Greiner DL, Blankenhorn EP.
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Viral antibody-free BBDR and WF rats never develop spontaneous diabetes. BBDR rats, however, develop autoimmune diabetes after perturbation of the immune system, e.g., by viral infection. We previously identified a disease-susceptibility locus in the BBDR rat, iddm4, which is associated with the development of autoimmune diabetes after treatment with polyinosinic:polycytidylic acid and an antibody that depletes ART2(+) regulatory cells. We have now developed lines of congenic WF.iddm4 rats and report that in an intercross of N5 generation WF.iddm4 rats, approximately 70% of animals either homozygous or heterozygous for the BBDR origin allele of iddm4 became hyperglycemic after treatment to induce diabetes. Fewer than 20% of rats expressing the WF origin allele of iddm4 became diabetic. Testing the progeny of various recombinant N5 WF.iddm4 congenic rats for susceptibility to diabetes suggests that iddm4 is centered on a small segment of chromosome 4 bounded by the proximal marker D4Rat135 and the distal marker D4Got51, an interval of <2.8 cM. The allele at iddm4 has 79% sensitivity and 80% specificity in prediction of diabetes in rats that are segregating for this locus. These characteristics suggest that iddm4 is one of the most powerful non-major histocompatibility complex determinants of susceptibility to autoimmune diabetes described to date.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401717&dopt=Abstract
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