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1 roglia and astrocytes, and included class II histocompatability antigens, the pro-inflammatory cytoki
4 pression during the differentiation of major histocompatability class 1 (MHC I)-restricted thymocytes
5 the invariant chain (li, CD74) of the major histocompatability class II complex (MHCII) undergoes in
11 rived from these exogenous antigens on major histocompatability complex (MHC) class I molecules and i
12 controlled by inhibitory receptors for major histocompatability complex (MHC) class I, including the
14 mpetence requires engagement of a self-major histocompatability complex (MHC) class I-specific inhibi
15 riptional activation of genes encoding major histocompatability complex (MHC) class II molecules and
16 ng cognate T cell-B cell interactions, major histocompatability complex (MHC) class II molecules tran
17 smaller peptides, and present them on major histocompatability complex (MHC) class II molecules with
19 naive CD8 T cells require self-peptide-major histocompatability complex (MHC) complexes for maintenan
22 To address this problem, the peptide-major histocompatability complex (MHC) ligand for a given popu
25 natural processing and presentation of major histocompatability complex (MHC) molecules as peptide by
26 recognize antigenic peptides bound to major histocompatability complex (MHC) molecules through commo
28 mocytes even in the absence of class I major histocompatability complex (MHC) proteins, ligands that
29 Genetic analysis of a mouse model of major histocompatability complex (MHC)-associated autoimmune t
30 thally irradiated mice receiving fully major histocompatability complex (MHC)-mismatched bone marrow
31 t disease (GVHD) after the infusion of major histocompatability complex (MHC)-mismatched donor bone m
32 clonal antibodies (Abs) that recognize major histocompatability complex (MHC)-presented tumor antigen
33 esponsiveness unless modulated by self-major histocompatability complex (MHC)-specific inhibitory rec
34 f the invariant chain (Ii) of class II major histocompatability complex (MHC-II) and aequorin was loc
35 enetic effects including those for the major histocompatability complex (MHC; particularly the HLA-DR
36 3, alpha-sarcomeric actin, CD3, CD11c, major histocompatability complex class I, hematoxylin-eosin).
40 cells; P<0.0001) and cells expressing major histocompatability complex class II (9 +/- 3 versus 40 +
42 n of CD8alpha and IL-12 p40 as well as major histocompatability complex class II and other costimulat
44 t facilitates folding and transport of major histocompatability complex class II molecules; here it i
46 presenting cells, measured as class II major histocompatability complex expressing cells, in lymph no
47 8 T cell responses in a cell contact-, major histocompatability complex I-, and influenza peptide-dep
48 tigen presentation, including class II major histocompatability complex molecules (HLA-DP, -DQ, and -
50 rately characterized the hypervariable major histocompatability complex region as well as demonstrati
52 ate considerably less than that of the major histocompatability complex, discovery of recent risk var
53 gainst CML cells but low reactivity to major histocompatability complex-matched normal bone marrow ce
55 d as recipients of syngeneic, multiple minor histocompatability (H)-disparate, or major histocompatib
57 Here, we show that Id3 is required for major histocompatability (MHC) class I- and class II-restricte