38 results on '"Keszei, Marton"'
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2. Generation of NK cells with chimeric-switch receptors to overcome PD1-mediated inhibition in cancer immunotherapy
3. A gain-of-function variant in the Wiskott-Aldrich syndrome gene is associated with a MYH9-related disease-like syndrome
4. IFNγ directly counteracts imatinib-induced apoptosis of primary human CD34+ CML stem/progenitor cells potentially through the upregulation of multiple key survival factors
5. Disease Progression of WHIM Syndrome in an International Cohort of 66 Pediatric and Adult Patients
6. P-020: PD1-based chimeric-switch receptor expressing NK cells recover from immune checkpoint inhibition in cancer
7. Overactive WASp in X-linked neutropenia leads to aberrant B-cell division and accelerated plasma cell generation
8. Constitutive activation of WASp in X-linked neutropenia renders neutrophils hyperactive
9. Combination of tyrosine kinase inhibitors and the MCL1 inhibitor S63845 exerts synergistic antitumorigenic effects on CML cells
10. Constitutive activation of WASp leads to abnormal cytotoxic cells with increased granzyme B and degranulation response to target cells
11. Constitutive activation of WASp in X-linked neutropenia renders neutrophils hyperactive
12. Wiskott-Aldrich syndrome gene mutations modulate cancer susceptibility in the p53±murine model
13. Nuclear Wiskott–Aldrich syndrome protein co-regulates T cell factor 1-mediated transcription in T cells
14. Slamf6 negatively regulates autoimmunity
15. Broad-spectrum antibodies against self-antigens and cytokines in RAG deficiency
16. Deletion of Wiskott–Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells
17. Broad-spectrum antibodies against self-antigens and cytokines in RAG deficiency
18. Deletion of WASp and N-WASp in B cells cripples the germinal center response and results in production of IgM autoantibodies
19. The cell surface receptor Slamf6 modulates innate immune responses during Citrobacter rodentium-induced colitis
20. Congenital Defects in Neutrophil Dynamics
21. SAP modulates B cell functions in a genetic background-dependent manner
22. Expansion of an osteopontin‐expressing T follicular helper cell subset correlates with autoimmunity in B6.Sle1b mice and is suppressed by the H1‐isoform of the Slamf6 receptor
23. SAP expression in invariant NKT cells is required for cognate help to support B-cell responses
24. NKT cells support B lymphocyte functions independently of expression of the adapter SAP. (106.45)
25. The H1-isoform of the cell surface receptor Slamf6 suppresses expansion of PD-1+ OPN+ CD4+ T Follicular Helper cells in the lupus-prone B6.Sle1b mice. (123.5)
26. Wiskott-Aldrich syndrome protein (WASP) and N-WASP are critical for peripheral B-cell development and function
27. Cutting Edge: Protein Phosphatase 2A Confers Susceptibility to Autoimmune Disease through an IL-17–Dependent Mechanism
28. B cell–intrinsic deficiency of the Wiskott-Aldrich syndrome protein (WASp) causes severe abnormalities of the peripheral B-cell compartment in mice
29. Cutting Edge: An NK Cell-Independent Role for Slamf4 in Controlling Humoral Autoimmunity
30. A novel isoform of the Ly108 gene ameliorates murine lupus
31. SLAM is a microbial sensor that regulates bacterial phagosome functions in macrophages
32. Expansion of immunoglobulin-secreting cells and defects in B cell tolerance in Rag-dependent immunodeficiency
33. SLAM family receptors and the SLAM-associated protein (SAP) modulate T cell functions
34. Homozygous DNA ligase IV R278H mutation in mice leads to leaky SCID and represents a model for human LIG4 syndrome
35. Defects of B Cell Tolerance and Expansion of Immunoglobulin Secreting Cells in Rag-dependent Immunodeficiency
36. F.121. B Cell-mediated Autoimmunity in Hypomorphic rag1 and lig4 Mouse Mutants as Models for Human Leaky SCID
37. HtrA1 is a novel mast cell serine protease of mice and men
38. Progesterone-Induced Blocking Factor Activates STAT6 via Binding to a Novel IL-4 Receptor
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