mertk apc  (R&D Systems)

Journal: PLoS Pathogens

Article Title: GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

doi: 10.1371/journal.ppat.1009176

Figure Lengend Snippet: A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. TYRO3, AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.

Article Snippet: Rabbit anti-human TYRO3 (Novus Biological), biotin-conjugated goat anti-human AXL, and APC anti-human MERTK mAb IgG1 (R&D Systems) were used to evaluate TAM receptor expression after fixation and permeabilization (Cytofix/Cytoperm Kit, BD Bioscience, San Diego, CA, USA).

Techniques: Expressing, Flow Cytometry, Staining, Control, Infection

Journal: PLoS Pathogens

Article Title: GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

doi: 10.1371/journal.ppat.1009176

Figure Lengend Snippet: The host type 2 immune response is elicited to clear parasitic helminth infections; however, the co-evolution of these parasites has promoted a variety of mechanisms to oppose and redirect immune responses by manipulating immune cell programming and function. Integrating our results with the current knowledge, we propose that gastrointestinal ( 1 ) helminths infections can enhance the regulatory axis of TAM receptors (TYRO3, AXL, and MERTK) in peripheral blood ( 2 ) CD11b high and CD1c high cells, and their ligand GAS6 in CD4 + T cells of patients with MS. This negative regulatory pathway could be essential for dampening co-stimulatory signals (CD40, CD80, and CD86) of antigen-presenting cells and controlling the pathological Th17 (pTh17) response at secondary lymphoid organs ( 3 ). The active chronic infection resets T helper response toward Th2/regulatory signals, limiting pathological Th17 (pTh17) effector response. This reprogramming of CD4 + T cells and GAS6 signaling under a helminth-induced type 2 environment could be essential for maintaining the balance between CD4 + IL-10 + and Th17 cells and reducing inflammatory IL-17 and IFNγ signals in the central nervous system ( 4 ). In summary, GAS6 tempers not only the innate immune response but also regulates Th17 development in an autocrine/paracrine manner.

Article Snippet: Rabbit anti-human TYRO3 (Novus Biological), biotin-conjugated goat anti-human AXL, and APC anti-human MERTK mAb IgG1 (R&D Systems) were used to evaluate TAM receptor expression after fixation and permeabilization (Cytofix/Cytoperm Kit, BD Bioscience, San Diego, CA, USA).

Techniques: Infection