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T Cells:Regulation and Cellular Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The CD6 molecule belongs to the same family of proteins as CD5. CD6 has Mr 130 kDa and is found on thymic and peripheral T cells, a B cell subset, and certain cells of the central nervous system. As with CD5, binding of CD6 induces calcium mobilization within the cell, and this can augment activation via other molecules such as CD3. CD6 is also a substrate for protein tyrosine kinases, its ligand is unknown.
Marrow Purging And Stem Cell Preparation
Published in Siegfried Matzku, Rolf A. Stahel, Antibodies in Diagnosis and Therapy, 2019
Denis C. Roy, Nadine Beauger, Martin Gyger
Depletion of CD6+ (anti-T12) T-cell was attempted by Ritz et al. in order to eliminate “mature” T lymphocytes of the marrow graft prior to allogeneic PCT (Roy et al., 1990b; Soiffer et al., 1992). Such an approach spares NK cells and a small proportion of T-cells, CD4+ or CD8+ (Rohatiner et al., 1986; Rasmussen et al., 1994). Champlin et al. rather opted to eliminate CD8+ T-cells from the marrow graft, sparing CD4+ T cells and a majority of NK cells (Champlin et al., 1990). In both instances, such efforts at selective T-cell depletion resulted in a low incidence of GVHD (Champlin et al., 1990; Soiffer et al., 1997). In addition, graft rejection, which was previously found to be a major problem in non-selective T-cell depleted transplants, occurred with an incidence comparable to that observed in transplants with unmanipulated marrow grafts (Soiffer et al., 1992; Champlin et al., 1990; Voltarelli et al., 1990; Soiffer et al., 1997). Mixed chimerism was documented in 51% of patients receiving CD6-depleted marrow grafts, and it correlated with lower numbers of CD4+ cells early post-PCT, but not with relapse, survival and disease-free-survival (Roy et al., 1990b). These results suggest that the subset of cells responsible for the GVL effect is distinct from those that may be responsible for preventing recurrence of normal recipient hematopoiesis.
Henipaviruses
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Olivier Escaffre, Viktoriya Borisevich, Barry Rockx
In addition, NiV-M can productively infect porcine peripheral blood monocytes, CD+6CD+8T lymphocytes, and NK cells. Infection of T cells expressing CD6, a strong ligand for the activated leukocyte cell adhesion molecule (ALCAM) which is highly expressed on the microvascular endothelial cells of the blood–air and the blood–brain barriers (BBBs), may explain the preferential tropism of NiV-M for small blood vessels of the lung and brain.67 Interestingly, human lymphocytes and monocytes are not permissive for NiV-M. Despite the absence of infection, lymphocytes could efficiently bind NiV-M and transfer infection to endothelial and Vero cells.68 In hamsters, such NiV-loaded mononuclear leukocytes transfer lethal NiV infection into naive animals, demonstrating efficient virus transinfection in vivo.
Anti-CD6 mAbs for the treatment of psoriasis
Published in Expert Opinion on Biological Therapy, 2020
Sunil Dogra, Shabeer D, Murlidhar Rajagopalan
CD6 is a cell surface glycoprotein expressed by most T cells and a subset of B cells that has incompletely-defined roles in regulation of lymphocyte development, selection, activation and differentiation. There is emerging evidence to implicate CD6 and its ligands in the pathogenesis and potentially the treatment of inflammatory and autoimmune diseases, like psoriasis and multiple sclerosis. Itolizumab is a humanized monoclonal antibody specific for human CD6, developed from its parent murine antibody, the IOR-T1 mAb at the Center of Molecular Immunology in Havana, Cuba. Itolizumab was commercially developed and released by Biocon in India under the brand name ALZUMAb in 2013 to be used in moderate to severe plaque psoriasis after approval by DCGI (Drug Controller General of India). Biocon collaborated with Equillium in 2017 to develop and commercialize itolizumab in Australia and New Zealand for a range of disorders including autoimmune diseases. Equillium had originally secured exclusive rights to develop and commercialize itolizumab for the US and Canada markets in May 2017. In addition to the EQUIP trial [61] in uncontrolled asthma, Equillium conducted Itolizumab’s Phase 1b clinical proof-of-concept trials for the treatment of acute graft versus host disease (aGVHD) and lupus nephritis (LN). Itolizumab has been awarded the fast track approval by the U.S. Food and Drug Administration (FDA) for treating aGVHD and LN. It has also received an Orphan Drug designations for the prevention and treatment of aGVHD [62].