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Background/Aims: The influence of lymphocytotoxic crossmatch on survival or acute rejection in liver transplantation remains controversial. Data regarding graft survival and acute rejection of living donor liver transplantation (LDLT) are limited. Methods: We retrospectively examined the influence of a positive T or B lymphocytotoxic crossmatch on survival and acute rejection in patients using a database of 414 consecutive LDLT cases. Results: The rejection-free rate at 90 days after LDLT was lower in patients that were T crossmatch-positive compared to patients that were both T and B crossmatch-negative (52 vs. 74%, p = 0.03). No patients with a positive lymphocytotoxic crossmatch died due to immunologic causes. The crossmatch results had no effect on graft survival. Conclusion: In the positive crossmatch groups, there was no acute rejection that was untreatable or that caused graft loss. These findings indicate that a positive crossmatch graft should not be considered a contraindication for LDLT. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

We aimed at investigating the distribution of various types of immunoregulatory T cells in the peripheral blood of patients with Hodgkin’s lymphoma (HL) (n = 94) being in the state of long-lasting complete remission using flow cytometry. Healthy patients (n = 41) as ‘negative’ and patients in complete remission with breast cancer (n = 47) as ‘positive’ controls were investigated in the study. We found significant elevations in the number of CD4+CD25high naturally occurring regulatory T cells, CD4+/intracellular IL-10+ (Tr1) and CD8+/intracellular IL-10+ T cells in HL compared to the healthy controls. In carcinoma patients, however, the number of Tr1 and CD8+/IL-10+ T cells was higher than that in the other two groups. The increase in the number of CD4+CD25high T cells seems to be characteristic of HL compared to the two other types of regulatory T cells. This change exists for a long time and it seems to be a characteristic of HL and independent of the types of therapy and the duration of time since therapy. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Continuous exposure of sensitized mice to an innocuous antigen, such as OVA, does not lead to chronic airway eosinophilia, but induces antigen unresponsiveness and resolution of the inflammatory response. In this study we explored mechanisms underlying attenuation of the airway inflammatory response, assessed whether the phenomenon is strain-specific, and determined its consequences to airway physiology. Methods: Mice were sensitized and exposed to OVA for two and four weeks. Analysis involved BAL, flow cytometry, adoptive transfer of OVA specific CD4 T cells, ex vivo cytokine expression and response to methacholine challenge. Results: Chronic exposure to antigen resulted in decreased eosinophilia in 5 different mouse strains. Likewise, numbers of lung CD4 T cells expressing activation and Th2 markers sharply declined following continuous OVA exposure. Transfer studies using OVA TcR transgenic cells revealed that the contraction of lung T cells included antigen-specific cells. Systemically, we observed a loss of Th2 memory effector function. Finally, we observed significantly attenuated airway hyper-responsiveness (AHR) in chronically exposed animals. Conclusions: Attenuation of airway eosinophilia in response to chronic OVA exposure is independent of genetic background. Airway eosinophilia, but not systemic responses, correlates with and is predictive for airway hyperresponsiveness. Our study contributes to the understanding of immune regulatory processes controlling antigen-driven airway inflammatory responses. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The implementation of highly active antiretroviral therapy (HAART) in patients with progressive HIV-1 disease has resulted in a marked reduction of HIV-1-associated morbidity and mortality. In fact, the risk of HAART responders to develop opportunistic infections becomes similar to that of long-term nonprogressors (LTNPs). Methods: Reasoning that HAART may ultimately have consequences on both the quantity and quality of immune responses of a HIV-1-infected person, we assessed CD4+ and CD8+ T cell subsets in HAART recipients over a time period of 15 months and compared them to the lymphocyte phenotype of LTNPs and healthy controls. Evaluations included quantitative determinations of memory (CD45RO+CD62L–), naive (CD45RO–CD62L+), effector (CD27–, CD28–) and activated (HLA-DR+, CD38+, CD95+) CD4+ and CD8+ lymphocytes. The T cell function was assayed by skin tests. Results: Compared to healthy persons, treatment-naive patients with progressive disease exhibited a considerable reduction of CD4+ T cells with many of the remaining T cells showing signs of activation at baseline. CD8+ T cells were greatly increased in number, mainly because of an expansion of CD28– effector and memory CD8+ T cells. LTNPs, in contrast, had stable CD4+ and elevated CD8+ T cell counts, the latter being mainly due to a marked increase in CD27– effector cells. Essentially, the same immunophenotype was seen in HAART responders after 15 months of treatment when compared to LTNPs. Conclusions: It is tempting to speculate that a HAART-induced reduction in viral load may influence the immune system’s capacity to mount protective responses to pathogenic microorganisms.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]