[Human milk, immune responses and health effects]
[Article in Norwegian]
Løland BF, Baerug AB, Nylander G.
Nasjonalt kompetansesenter for amming, Kvinneklinikken, Rikshospitalet-Radiumhospitalet, 0027 Oslo. beate.fossum.loland@rikshospitalet.no
BACKGROUND: Besides providing optimal nutrition to infants, human milk contains a multitude of immunological components. These components are important for protection against infections and also support the development and maturation of the infant's own immune system. This review focuses on the function of some classical immunocomponents of human milk. Relevant studies are presented that describe health benefits of human milk for the child and of lactation for the mother. MATERIAL AND METHODS: Relevant articles were found mainly by searching PubMed. RESULTS AND INTERPRETATION: Humoral and cellular components of human milk confer protection against infections in the respiratory,-- gastrointestinal--and urinary tract. Human milk also protects premature children from neonatal sepsis and necrotizing enterocolitis. There is evidence that human milk may confer long-term benefits such as lower risk of certain autoimmune diseases, inflammatory bowel disease and probably some malignancies. Human milk possibly affects components of the metabolic syndrome. Recent studies demonstrate long-term health benefits of lactation also for the mother. A reduced incidence of breast cancer is best documented. An increasing number of studies indicate protection against ovarian cancer, rheumatoid arthritis and type II diabetes.
PMID: 17895946 [PubMed - indexed for MEDLINE]
Peptide-MHC Class II Dimers as Therapeutics to Modulate Antigen-Specific T Cell Responses in Autoimmune Diabetes.
Masteller EL, Warner MR, Ferlin W, Judkowski V, Wilson D, Glaichenhaus N, Bluestone JA.
Diabetes Center, University of California, San Francisco, CA 94143. Centre National de la Recherche Scientifque, University of Nice-Sophia Antipolis, Valbonne, France. Torrey Pines Institute for Molecular Studies, San Diego, CA 92121.
Type 1 diabetes is an autoimmune disorder caused by autoreactive T cells that mediate destruction of insulin-producing beta cells of the pancreas. Studies have shown that T cell tolerance can be restored by inducing a partial or altered signal through the TCR. To investigate the potential of bivalent peptide-MHC class II/Ig fusion proteins as therapeutics to restore Ag-specific tolerance, we have developed soluble peptide I-A(g7) dimers for use in the nonobese diabetic mouse model of diabetes. I-A(g7) dimers with a linked peptide specific for islet-reactive BDC2.5 TCR transgenic CD4(+) T cells were shown to specifically bind BDC2.5 T cells as well as a small population of Ag-specific T cells in nonobese diabetic mice. In vivo treatment with BDC2.5 peptide I-A(g7) dimers protected mice from diabetes mediated by the adoptive transfer of diabetogenic BDC2.5 CD4(+) T cells. The dimer therapy resulted in the activation and increased cell death of transferred BDC2.5 CD4(+) T cells. Surviving cells were hypoproliferative to challenge by Ag and produced increased levels of IL-10 and decreased levels of IFN-gamma compared with cells from control I-A(g7) dimer-treated mice. Anti-IL-10R therapy reversed the tolerogenic effects of the dimer. Thus, peptide I-A(g7) dimers induce tolerance of BDC2.5 TCR T cells through a combination of the induction of clonal anergy and anti-inflammatory cytokines.
J Immunol. 2003 Nov 15;171(10):5587-95.