Polyclonal hypergammaglobulinemia and high smooth-muscle autoantibody titers with specificity against filamentous actin: consider visceral leishmaniasis, not just autoimmune hepatitis.
Exome Sequencing Identifies Two Variants of the Alkylglycerol Monooxygenase Gene as a Cause of Relapses in Visceral Leishmaniasis in Children, in Sudan.
Levels of HDL, LDL fraction, and apolipoprotein A1 in ZVL patients' sera were lower than those of healthy individuals' sera, except for the mean level of VLDL.
Asparaginase, a pivotal enzyme of the aspartate metabolic pathway is present as two variants in Leishmania donovani, causative agent of visceral leishmaniasis (VL).
Buparvaquone (BPQ), a hydroxynapthoquinone with in vitro activity in the nanomolar range, failed to clinically translate as a viable treatment for visceral leishmaniasis due to its poor oral bioavailability limited by its poor aqueous solubility (BCS Class II drug).
Further, the increased levels of TGF-β and caspase 3 at 90th day suggested TGF-β mediated apoptotic cell death of renal and other cells during later stages of disease that may eventually result in release of host and parasitic factors in urine during visceral leishmaniasis.
MCP-1 was also significantly elevated in all patients cured of visceral leishmaniasis (VL), unlike IL-2, indicating the specific memory response generated against <i>Leishmania</i>.
In visceral leishmaniasis (VL), cellular immunosuppression is mediated by impaired DC migration due to the decreased chemokine secretion by endothelium and to the reduced DCs CCR7 expression.
Further, we found reduced expression of the chemokine receptors CXCR1, CXCR2, CXCR3 and CCR2, but increased expression of CCR7 on VL PBMC, compared to endemic healthy controls.
Active cases of VL was observed with 2.91-fold increased mean florescence intensity (MFI) of LFA-3 expression on CD14(+) cells compared to healthy control (p = 0.0001).
Recent studies have raised the possibility of using immunohistochemistry in the diagnosis of visceral leishmaniasis with labeling of amastigotes by the anti-CD1a antibody.
Here, we examined the role of PD1/PDL-1 in the pathogenesis of VL by using a murine model of VL.Our data indicate that <i>L. donovani</i> is able to elicit initial expansion of gamma interferon-producing CD4<sup>+</sup> Th1 and CD8<sup>+</sup> T cells at day 7 postinfection (p.i.); however, the frequency of those cells and inflammatory response decreased at day 21 p.i., despite persistence of parasites.
In contrast to naïve mice, where most long-term hematopoietic stem cells (LT-HSCs; LSK CD150+ CD34- CD48- cells) in bone marrow (BM) are quiescent, we found that during Leishmania donovani infection most LT-HSCs had entered cell cycle.
Our results in HIV coinfected patients, correspond with the postulated protective role of sCD40L in VL and underline the importance of the CD40-CD40L pathway in resistance against the parasite.
Our results in HIV coinfected patients, correspond with the postulated protective role of sCD40L in VL and underline the importance of the CD40-CD40L pathway in resistance against the parasite.
The mean florescence intensity (MFI) of CD58 but not of CD2 was twofold higher on CD56<sup>+</sup> cells during VL, but was down-regulated after treatment.
Active cases of VL was observed with 2.91-fold increased mean florescence intensity (MFI) of LFA-3 expression on CD14(+) cells compared to healthy control (p = 0.0001).
The present study has enumerated the effect of 61 kDa recombinant Leishmania donovani co-factor-independent phosphoglycerate mutase (rLd-iPGAM) on mononuclear cells of healthy and treated visceral leishmaniasis subjects as well as on THP-1 cell line. rLd-iPGAM stimulation induced higher expression of interleukin-1β (IL-1β) in the phagocytic cell, its receptor and CD69 on T-cell subsets.
However, lymphocytes from sVL stimulated with SLA had lower percentages of CD4<sup>+</sup> and CD8<sup>+</sup> cells expressing CD69 and CD8<sup>+</sup> cells expressing CD25, with no release of interferon-γ or tumor necrosis factor. sVL subjects had lower percentage of memory cells (CD4<sup>+</sup> CD45RO+), ex vivo, without SLA stimulation than RecVL, LST+, or LST- (<i>P</i> = 0.0022).