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Ann N Y Acad Sci. 2002 Apr;958:39-46.
The gut immune system and type 1 diabetes.

Vaarala O.

Department of Molecular Medicine, National Public Health Institute, Biomedicum, 00251 Helsinki, Finland. outi.vaaraltl.fi

Accumulating data suggest that the gut immune system plays a role in the development of autoimmune diabetes: (1) Diet modifies the incidence of autoimmune diabetes and the phenotype of the islet-infiltrating T cells in the animal models of human type 1 diabetes; (2) gut-associated homing receptor beta7-integrin is found on the islet-infiltrating T cells in both human type 1 diabetes and in the animal models of autoimmune diabetes; (3) mesenterial lymphocytes from young NOD mice are able to transfer diabetes to healthy recipients; (4) autoantigen feeding modifies the disease development in the animal models (prevents or accelerates autoimmune diabetes). In humans, a link between the gut immune system and type 1 diabetes has also been suggested. Early introduction of cow milk formulas in infancy may increase the risk of type 1 diabetes. We have demonstrated that primary immunization to a beta cell-specific autoantigen, insulin, occurs in the gut by exposure to cow milk formulas, which contain immunogenic bovine insulin. The induced antibody and T cell responses to bovine insulin cross-react with human insulin. In children at genetic risk who developed beta cell autoimmunity, bovine insulin-binding antibodies increased during follow-up in contrast to autoantibody-negative children. This suggests that insulin-specific immune response induced by dietary insulin may not be controlled in children prone to beta cell autoimmunity. The gut immune system has a key role in controlling insulin-specific immunity induced by dietary insulin. Indeed, indications for aberrant function of the gut immune system have been reported in type 1 diabetes, such as intestinal immune activation and increased intestinal permeability. Research on the gut immune system in human type 1 diabetes is needed to reveal the role of oral immunity in this disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021082&dopt=Abstract

Ann N Y Acad Sci. 2002 Apr;958:431-5.
Could parenting stress and lack of support/confidence function as mediating mechanisms between certain environmental factors and the development of autoimmunity in children?: a study within ABIS.

Sepa A, Frodi A, Ludvigsson J.

Division of Pediatrics, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, University of Linkoping, Linkoping, Sweden. anneli.sepmk.liu.se

Despite extensive research, the etiology of type 1 diabetes is still to a large extent unknown. We would like to propose psychoimmunology as one possible pathway. Psychological mechanisms are directly linked to hormonal and nervous signals, which increase the need for insulin and affect the immune system. Disparate factors of social, environmental, and medical character have been associated with the onset of type 1 diabetes or with the autoimmune process leading to the disease-for instance, parental age, maternal infections, delivery mood, need for neonatal intensive care, and low socioeconomic status. Our results, based on the analyses of 4337 nonselected newborn children and their mothers, show that all these risk factors were also associated with psychological mechanisms (defined as lack of social support/confidence and high parenting stress). These results support the hypothesis of psychological mechanisms as mediating variables between a number of disparate risk factors and the development of type 1 diabetes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021156&dopt=Abstract

J Virol. 2002 Jun;76(12):6027-36.
Detection of CD4(+)- and CD8(+)-T-cell responses to human papillomavirus type 1 antigens expressed at various stages of the virus life cycle by using an enzyme-linked immunospot assay of gamma interferon release.

Steele JC, Roberts S, Rookes SM, Gallimore PH.

Cancer Research UK Institute for Cancer Studies, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom. j.c.steelham.ac.uk

Human papillomavirus (HPV) antigens are expressed in epithelial cells at different stages of differentiation, and this may affect how they are handled by the immune system. We assessed the relative immunogenicities of four different HPV type 1 proteins: E6 and E7, which are made early in basal or parabasal cells; E4, which is made suprabasally in differentiating cells; and L1, a late protein which appears in the highly differentiated upper spinous layers. Pools of 15-mer peptides covering the primary sequences of all four proteins were used to screen 15 normal donors in enzyme-linked immunospot assays of gamma interferon release for both CD4(+)- and CD8(+)-T-cell reactivities. CD8(+)-T-cell responses were detected to the L1 protein in 7 of the 15 samples examined. No responses to E6, E7, or E4 were detected. CD4(+)-T-cell reactivities were again detected in 7 of the 15 donors. A broader spectrum of responses to E6 (three of seven), E4 (six of seven), and L1 (three of seven) was apparent, but there was no reactivity to E7. The predominant CD4(+) response was to E4. Reactivities were seen in some cases to corresponding regions on other common HPV types but were probably due to a multiple infection rather than to a cross-reaction. Antibodies to HPV1 virus-like particles were detected in 12 of the 15 (80%) donors, but antibody status did not correlate with T-cell reactivity. The differences in the relative immunogenicities of the four proteins revealed in this study are discussed in relation to how they may be processed and presented to the immune system by differentiating epithelial cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021335&dopt=Abstract

Int Arch Allergy Immunol. 2002 Apr;127(4):316-21.
Substance P induced preprotachykinin-a mRNA, neutral endopeptidase mRNA and substance P in cultured normal fibroblasts.

Bae SJ, Matsunaga Y, Takenaka M, Tanaka Y, Hamazaki Y, Shimizu K, Katayama I.

Department of Dermatology, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan. s-jbaet.nagasaki-u.ac.jp

In certain skin diseases, stress can modulate the induction and/or progression of cutaneous manifestations. However, little is known about the circuit in neuroendocrine and in the immune systems of the skin. To address this question, we have analyzed the regulatory mechanisms of autocrine induction of substance P (SP) by cultured normal human fibroblasts that compose the major population of the skin and might augment stress-induced skin inflammatory responses. In nonstimulated conditions, normal fibroblasts express a moderate amount of preprotachykinin-A (PPT-A), a precursor of SP mRNA, and exogenous SP significantly upregulated PPT-A mRNA expression. Maximum response of SP peptide and SP mRNA in fibroblasts was observed 1-3 h after stimulation with SP. In contrast, the expression of neutral endopeptidase (NEP), a cell surface peptide with hydrolyzing activity of SP, was increased in fibroblasts stimulated with SP after 24 h. The administration of NEP inhibitor (phosphoramidon) to the fibroblasts induced higher SP production. In addition, the neurokinin (NK) receptor antagonists (spantide, FK224 and FK888) and protein synthesis inhibitor (cycloheximide) inhibited SP production by 30-40% of control response. In immunostaining study, specific cytoplasmic staining of SP was observed in fibroblasts stimulated with SP. Finally, we confirmed that the nucleotide sequence of the PPT-A expressed in fibroblasts perfectly corresponded to the gene bank human PPT-A cDNA. This is the first report that SP mRNA, NEP mRNA and SP peptide can be induced by normal human skin fibroblasts in response to exogenous SP, and that fibroblast-derived SP might play an important role in the induction and acceleration of certain cutaneous diseases. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021551&dopt=Abstract

J Math Biol. 2002 May;44(5):395-426.
Analysis of a mathematical model for the growth of tumors under the action of external inhibitors.

Cui S.

Department of Mathematics, Zhongshan University, Guangzhou, Guangdong 510275, P. R. China. mcinssu.edu.cn

In this paper we make rigorous analysis to a mathematical model for the growth of nonnecrotic tumors under the action of external inhibitors. By external inhibitor we mean an inhibitor that is either developed from the immune system of the body or administered by medical treatment to distinguish with that secreted by tumor itself. The model modifies a similar model proposed by H. M. Byrne and M. A. J. Chaplain. After simply establishing the well-posedness of the model, we discuss the asymptotic behavior of its solutions by rigorous analysis. The result shows that an evolutionary tumor will finally disappear, or converge to a stationary state (dormant state), or expand unboundedly, depending on which of the four disjoint regions Delta1,..., Delta4 the parameter vector (A1,A2) belongs to, how large the scaled apoptosis number;sigma is, and how large the initial radius R(0) of the tumor is. Finally, we discuss some biological implications of the result, which reveals how a tumor varies when inhibitor supply is increased and nutrient supply is reduced.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12021982&dopt=Abstract

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