High-dose immunosuppression and AHST were performed with acceptable toxicity in a small number of patients with newly diagnosed type 1 DM. With AHST, beta cell function was increased in all but 1 patient and induced prolonged insulin independence in the majority of the patients.

CCUMULATED CLINICAL EXPErience indicates that there is an inverse association between beta-cell function and chronic complications of type 1 diabetes mellitus (DM)-the higher the Cpeptide levels (an indirect measure of viable beta-cell function), the lower the incidence of microvascular complications of type 1 DM. 1 Since the establishment of the autoimmune etiology of type 1 DM in the late 1970s, many clinical trials analyzing the effects of different types of immune interventions demonstrated that beta-cell preservation is an achievable target in different degrees. 2,3 Based on the theory of possible reconstitution of immune tolerance after "immunologic reset" with autologous nonmyeloablative hematopoietic stem cell transplantation (HSCT), 4 in 2007, we reported a phase 1/2 trial evaluating the safety and metabolic effects of autologous nonmyeloablative HSCT in 15 patients with newly diagnosed type 1 DM. 5 The majority of pa-Author Affiliations are listed at the end of this article.

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This study analyzed the association of periodontal disease (PD) and rheumatoid arthritis (RA). seventy-five 35-60-year-old patients were assigned to 5 groups according to the presence (+) or not (-) of PD and RA and the treatment received (TR+) or not (TR-) for PD. Group 3 uses total prosthesis (TP). Clinical and laboratory evaluations were performed at baseline, 3 and 6 months of follow-up by probing pocket depth, bleeding on probing and plaque index for PD, hAQ, DAs28, sF-36 and laboratory: AAG, esR, CRP for RA. statistically significant differences for PD after 3 (p=0.0055) and after 6 months (p=0.0066) were obtained in Group 1 (RA+PD+TR+) and 2(RA+PD+TR-); significant reduction in the % of BoP after 6 months (p=0.0128) and significant reduction in the % of Pl after 3 (p=0.0128) and 6 months (p=0.0002) in Group 1. statistically significant differences between Groups 1 and 3 (RA+TP) for DAs28 at baseline and after 3 months were observed, but not after 6 months. No other parameters for RA were significantly affected. The relationship between RA and PD disease activities is not clear, but the importance of periodontal treatment in the control of inflammation to avoid tooth extraction is evident.

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Current approaches aiming to cure type 1 diabetes (T1D) have made a negligible number of patients insulin-independent. In this review, we revisit the role of stem cell (SC)-based applications in curing T1D. The optimal therapeutic approach for T1D should ideally preserve the remaining β-cells, restore β-cell function, and protect the replaced insulin-producing cells from autoimmunity. SCs possess immunological and regenerative properties that could be harnessed to improve the treatment of T1D; indeed, SCs may reestablish peripheral tolerance toward β-cells through reshaping of the immune response and inhibition of autoreactive T-cell function. Furthermore, SC-derived insulin-producing cells are capable of engrafting and reversing hyperglycemia in mice. Bone marrow mesenchymal SCs display a hypoimmunogenic phenotype as well as a broad range of immunomodulatory capabilities, they have been shown to cure newly diabetic nonobese diabetic (NOD) mice, and they are currently undergoing evaluation in two clinical trials. Cord blood SCs have been shown to facilitate the generation of regulatory T cells, thereby reverting hyperglycemia in NOD mice. T1D patients treated with cord blood SCs also did not show any adverse reaction in the absence of major effects on glycometabolic control. Although hematopoietic SCs rarely revert hyperglycemia in NOD mice, they exhibit profound immunomodulatory properties in humans; newly hyperglycemic T1D patients have been successfully reverted to normoglycemia with autologous nonmyeloablative hematopoietic SC transplantation. Finally, embryonic SCs also offer exciting prospects because they are able to generate glucose-responsive insulin-producing cells. Easy enthusiasm should be mitigated mainly because of the potential oncogenicity of SCs.

Current understanding of the role of several cancer risk factors is more comprehensive, as reported for a number of sites, including the brain, colon, breasts, and ovaries. Despite such advances, the incidence of breast cancer continues to increase worldwide. Signals from the microenviroment have a profound influence on the maintenance or progression cancers. Although T cells present the most important immunological response in tumor growth in the early stages of cancer, they become suppressive CD4(+) and CD8(+) regulatory T cells (Tregs) after chronic stimulation and interactions with tumor cells, thus promoting rather than inhibiting cancer development and progression. Tregs have an important marker protein which is FoxP3, though it does not necessarily confer a Treg phenotype when expressed in CD4(+) T lymphocytes. High Treg levels have been reported in peripheral blood, lymph nodes, and tumor specimens from patients with different types of cancer. The precise mechanisms by which Tregs suppress immune cell functions remain unclear, and there are reports of both direct inhibition through cell-cell contact and indirect inhibition through the secretion of anti-inflammatory mediators such as interleukin. In this review, we present the molecular and immunological aspects of Treg cells in the metastasis of breast cancer.