Background: L-selectin (CD62L) is a cell surface adhesion molecule recently shown to play a critical role in determining endometrial receptivity and implantation in humans. By contrast, the L-selectin ligand is missin...Background: L-selectin (CD62L) is a cell surface adhesion molecule recently shown to play a critical role in determining endometrial receptivity and implantation in humans. By contrast, the L-selectin ligand is missing from the rodent endometrium. Interestingly, CD62L (L-selectin)-deficient BALB/c mice delivered significantly higher numbers of viable offspring than wild type controls via mechanisms yet to be defined. Methods: Nulliparous CD62L-deficient (8-10-week-old, n = 25) or wild type (n = 18) females were mated with 43 age-matched males. Animals were sacrificed at gestational day (GD) 9.5. Tissue samples were analyzed by immunostaining and flow cytometry. Results: Mating wild type and CD62L-deficient BALB/c mice revealed that the increased birth rate was due to the CD62L deficiency in females. Flow cytometric analysis demonstrated significant differences in the number of natural killer (NK) cells present in the uterus of pregnant CD62L- deficient mice compared to controls. Immunohistochemistry confirmed NK cell accumulation at the fetal-maternal interface. Discussion: Uterine NK cells have been shown to peak at GD 8-10 at the fetal-maternal interface. NK cells might regulate mouse fertility rates by facilitating development of the maternal spiral arteries, thereby stimulating the formation of larger vessels that facilitate intrauterine survival, however, their role is not obligate to spiral artery development. Conclusions: Diminished CD62L expression modified immune cell trafficking into the uterus of pregnant mice generating a microenvironment primarily dominated by NK cells resulting in improved embryonic survival rates.展开更多
<strong>Backgrounds:</strong> Recent advances in post Kidney Transplantation (KT) care, have led to a dramatic improvement in short-term outcomes in order to achieve transplantation tolerance;including the...<strong>Backgrounds:</strong> Recent advances in post Kidney Transplantation (KT) care, have led to a dramatic improvement in short-term outcomes in order to achieve transplantation tolerance;including the ideal tool for clinical monitoring & new therapeutic line. This study was undertaken to analyze the CD62L in Kidney Transplant Recipients (KTRs) and to investigate its efficacy as a marker of good graft survival. <strong>Methods:</strong> Fifty pediatric KTRs and 12 healthy controls were included in the study, the frequency of T cell activation markers;CD62L was measured with flow cytometry after renal transplantation. Clinical, laboratory, immunosuppressive therapy data and graft function of transplant recipients were collected and correlated with their CD62L peripheral blood percentage. <strong>Results:</strong> The circulating CD62L% was significantly more in transplant recipients than controls (44.74% ± 17.45% vs. 33.36% ± 11.54%, p = 0.02). CD 62L% was more frequent in recipients of living related donors (p = 0.05), positively correlated with donor age (p = 0.04, r = -0.29<sup>*</sup>) and CD 4% (p = 0.000, r = 0.615). CD26L% did not show significant association with acute rejection or chronic rejection (p = 0.432, p = 0.91 respectively) or with graft function (serum creatinine or eGFR, p = 0.086, p = 0.988 respectively) or immunosuppressive medications. <strong>Conclusion:</strong> Peripheral CD62L% is increased after KT than healthy controls, however, it cannot reflect either clinical (serum creatinine and eGFR) or pathological renal graft injury. CD62L surface marker needs more analysis for its potential diagnostic and therapeutic implications as a Treg cell activation marker.展开更多
Background: A reduction in the expression of the pan T-cell markers CD7 and CD62L supports an endogenous T-cell dyscrasia. Previously, clone availability for CD62L restricted its application to frozen tissue sections....Background: A reduction in the expression of the pan T-cell markers CD7 and CD62L supports an endogenous T-cell dyscrasia. Previously, clone availability for CD62L restricted its application to frozen tissue sections. Materials and methods: A nonavidin/biotin technique to examine CD3, CD62L, and CD7 in paraffin formalin-fixed tissue in non-neoplastic and neoplastic T- cell infiltrates. Results: In the reactive group, CD62L manifested a 15 and 22% reduction in epidermal and dermal staining, respectively; there was a 42 and 31% reduction in epidermal and dermal CD7 staining. In lymphomatoid hypersensitivity, CD62L showed a 24 and 9% reduction in epidermal and dermal staining, respectively; CD7 staining demonstrated reduced staining by 70 and 66% in the epidermis and dermis. In the non-lymphomatous endogenous T-cell dyscrasia and lymphoma categories, an 80% diminution in CD62L and CD7 expression was seen. Conclusions: CD62L can be successfully applied in formalin- fixed tissue and exhibits enhanced specificity compared to CD7 in the evaluation of cutaneous T-cell infiltrates. Both CD62L and CD7 in paraffin-embedded, formalin- fixed tissue are useful diagnostic adjuncts, especially in regard to the discrimination of lymphomatoid hypersensitivity reactions from true endogenous T-cell dyscrasia.展开更多
文摘Background: L-selectin (CD62L) is a cell surface adhesion molecule recently shown to play a critical role in determining endometrial receptivity and implantation in humans. By contrast, the L-selectin ligand is missing from the rodent endometrium. Interestingly, CD62L (L-selectin)-deficient BALB/c mice delivered significantly higher numbers of viable offspring than wild type controls via mechanisms yet to be defined. Methods: Nulliparous CD62L-deficient (8-10-week-old, n = 25) or wild type (n = 18) females were mated with 43 age-matched males. Animals were sacrificed at gestational day (GD) 9.5. Tissue samples were analyzed by immunostaining and flow cytometry. Results: Mating wild type and CD62L-deficient BALB/c mice revealed that the increased birth rate was due to the CD62L deficiency in females. Flow cytometric analysis demonstrated significant differences in the number of natural killer (NK) cells present in the uterus of pregnant CD62L- deficient mice compared to controls. Immunohistochemistry confirmed NK cell accumulation at the fetal-maternal interface. Discussion: Uterine NK cells have been shown to peak at GD 8-10 at the fetal-maternal interface. NK cells might regulate mouse fertility rates by facilitating development of the maternal spiral arteries, thereby stimulating the formation of larger vessels that facilitate intrauterine survival, however, their role is not obligate to spiral artery development. Conclusions: Diminished CD62L expression modified immune cell trafficking into the uterus of pregnant mice generating a microenvironment primarily dominated by NK cells resulting in improved embryonic survival rates.
文摘<strong>Backgrounds:</strong> Recent advances in post Kidney Transplantation (KT) care, have led to a dramatic improvement in short-term outcomes in order to achieve transplantation tolerance;including the ideal tool for clinical monitoring & new therapeutic line. This study was undertaken to analyze the CD62L in Kidney Transplant Recipients (KTRs) and to investigate its efficacy as a marker of good graft survival. <strong>Methods:</strong> Fifty pediatric KTRs and 12 healthy controls were included in the study, the frequency of T cell activation markers;CD62L was measured with flow cytometry after renal transplantation. Clinical, laboratory, immunosuppressive therapy data and graft function of transplant recipients were collected and correlated with their CD62L peripheral blood percentage. <strong>Results:</strong> The circulating CD62L% was significantly more in transplant recipients than controls (44.74% ± 17.45% vs. 33.36% ± 11.54%, p = 0.02). CD 62L% was more frequent in recipients of living related donors (p = 0.05), positively correlated with donor age (p = 0.04, r = -0.29<sup>*</sup>) and CD 4% (p = 0.000, r = 0.615). CD26L% did not show significant association with acute rejection or chronic rejection (p = 0.432, p = 0.91 respectively) or with graft function (serum creatinine or eGFR, p = 0.086, p = 0.988 respectively) or immunosuppressive medications. <strong>Conclusion:</strong> Peripheral CD62L% is increased after KT than healthy controls, however, it cannot reflect either clinical (serum creatinine and eGFR) or pathological renal graft injury. CD62L surface marker needs more analysis for its potential diagnostic and therapeutic implications as a Treg cell activation marker.
文摘Background: A reduction in the expression of the pan T-cell markers CD7 and CD62L supports an endogenous T-cell dyscrasia. Previously, clone availability for CD62L restricted its application to frozen tissue sections. Materials and methods: A nonavidin/biotin technique to examine CD3, CD62L, and CD7 in paraffin formalin-fixed tissue in non-neoplastic and neoplastic T- cell infiltrates. Results: In the reactive group, CD62L manifested a 15 and 22% reduction in epidermal and dermal staining, respectively; there was a 42 and 31% reduction in epidermal and dermal CD7 staining. In lymphomatoid hypersensitivity, CD62L showed a 24 and 9% reduction in epidermal and dermal staining, respectively; CD7 staining demonstrated reduced staining by 70 and 66% in the epidermis and dermis. In the non-lymphomatous endogenous T-cell dyscrasia and lymphoma categories, an 80% diminution in CD62L and CD7 expression was seen. Conclusions: CD62L can be successfully applied in formalin- fixed tissue and exhibits enhanced specificity compared to CD7 in the evaluation of cutaneous T-cell infiltrates. Both CD62L and CD7 in paraffin-embedded, formalin- fixed tissue are useful diagnostic adjuncts, especially in regard to the discrimination of lymphomatoid hypersensitivity reactions from true endogenous T-cell dyscrasia.
