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A team of medical experts and international office of MHCII (Ebru Tok, Hashim Carikli and Prof Dr Polat) agreed to develop a potential collaborative model.
The phenotype analysis of Immature BMDC revealed that GM-[CSF.sup.lo] DC derived from culture as well as kit method expressed intermediate level of MHCII, decreased expression of CD86, and very low levels of CD40 (Figures 3 and 4).
Both lung- and bone marrow-purified [CD11b.sup.+][Gr-1.sup.+] and [CD11b.sup.+] [Gr-1.sup.-] myeloid cells were stained for CD80, CD86, MHCII, CD62L, and F4/80 for flow cytometry analysis.
Caption: Figure 1: Analysis of ROS formation 2h and maturation (high MHCII and CD86 expression) 24 h after stimulation of BM-DCs with (a) increasing concentrations of PDBu (0.01-1 [micro]M) or LPS (0.5-30 [micro]g/ml) or (b) PDBu (0.1 [micro]M), PMA (50 ng/ml), zymosan A (ZymA, 50 [micro]g/ml), LPS (1.5 [micro] g/ml), lipoteichoic acid (LTA, 10 [micro]g/ml), antiCD40 (10 [micro]g/ml), mrCD40L (0.5 [micro] g/ml) or TNF-[alpha]/IL-1[beta] (10 ng/ml each) by flow cytometry.
Effects of Ephedra Aconite Asarum Decoction on the Expression of CD83, MHCII, and CD80 on LPS-Induced DCs.
Ting, "Epigenetic regulation of MHCII and CIITA genes," Trends in Immunology, vol.
In this study, a DNA vaccine and its respective protein were constructed in which Foxp3 fused to Fc(IgG) can be efficiently captured and processed by DC via receptor mediated endocytosis and presented to MHCII and I (cross priming).
Specialized cells in the thymus interact with a molecule known as the Major Histocompatibility Complex class II (MHCII) to "teach" T cells to differentiate between normal tissues and organs, and foreign invaders.
The increase in CD4+ T cell responses by MHCII li is well known (Holst et al., 2008).
Major histocompatibility complex II (MHCII) overexpression has been previously shown to play a role in the activation of both the innate and adaptive immune responses to [alpha]-synclein aggregation in PD.
For example, alterations in immune homeostasis and signs of immune dysregulation such as increased expression of MHCII and inflammatory cytokines have been found in the intestines of both T1D patients and preclinical T1D models even before clinical onset of the disease [10-16].
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