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1 Ig heavy chain (IgH) isotypes (e.g., IgM, IgG, and IgE)
2 Ig heavy-chain variable region exons are assembled devel
3 Ig stripping combined with passive sensitization +/- oma
4 (cytotoxic T-lymphocyte-associated protein 4 Ig) is an emerging treatment in kidney transplantation.
5 The development of the fusion protein CTLA-4-Ig as an experimental and subsequent therapeutic tool is
8 cytotoxic T-lymphocyte-associated protein 4-Ig reducing disease symptoms and immunologic disturbance
9 cytotoxic T-lymphocyte-associated protein 4-Ig should be evaluated as a potential treatment of infla
12 tructural motifs located in the two adjacent Ig-like domains dictate the processing of CTDs by the T9
14 cess of somatic hypermutation (SHM) and also Ig class switching, can have a potent mutator phenotype
15 y, we aimed to evaluate whether this altered Ig repertoire interferes with the inflammatory responsiv
17 rial subunits that makes them peculiar among Ig-like domain-containing proteins is a conserved disulf
19 cells in thymus were mature and displayed an Ig gene repertoire that was similar to pediatric bone ma
20 afted B-1 cells in humanized mice exhibit an Ig-usage pattern comparable to B-1 cells in cord blood.
21 erized NOD mice transgenically expressing an Ig molecule representative of a large proportion of natu
24 e single-pass transmembrane proteins with an Ig-like domain, share the same subcellular distribution
25 ed a phylogenetic distance metric to analyze Ig heavy-chain transcript sequences in both young and el
26 reened a cohort of 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for ant
27 profile, as indicated by increased CD57 and Ig-like transcript 2 and an inability to produce IFN-gam
28 tosis, Fc receptor function, complement, and Ig regulation are enhanced in PBS-treated Nrf2 null gene
30 ing promotes plasma cell differentiation and Ig production, we investigated whether stromal expressio
31 also observed the codeposition of DNAJB9 and Ig-gamma Overall, these findings indicate that DNAJB9 is
33 l activation induces terminal maturation and Ig isotype class switch (class switch recombination [CSR
35 nexpectedly that the leucine-rich repeat and Ig domain protein 1 (LINGO1) is expressed in over 90% of
36 ly demonstrated that leucine-rich repeat and Ig-like domain-containing Nogo receptor interacting prot
39 ol of the Fc-associated glycan structure and Ig subclass composition on the one hand and selective Fc
41 with median survivals close to 25 years, and Ig-mutated CLL, where have more aggressive disease with
43 s analysis of immunoglobulin (referred to as Ig-seq) coupled with high-throughput sequencing of trans
45 development of a novel flow cytometry-based Ig capture assay (ICA) for the identification and sortin
47 Immunogenetic studies of the clonotypic BCR Ig of CLL subset #4 suggested a resemblance with B cells
50 ler (NK) cell inhibitory sialic acid-binding Ig-like lectin (Siglec) receptors, and enhanced binding
52 if ligand 18 (PARC), and sialic acid-binding Ig-like lectin 14 (SIG14) were significantly modulated i
58 the sulfotyrosine-binding pocket by CCR5mim2-Ig was sufficient for promoting CD4bs antibody binding t
60 re more efficiently neutralized by human CD4-Ig (huCD4-Ig) than by the same molecule bearing rhesus C
61 without altering neutralization by human CD4-Ig, SIV neutralizing antibodies, or sera from SIV-infect
63 its neutralization sensitivity to rhesus CD4-Ig without altering neutralization by human CD4-Ig, SIV
65 ll analysis to interrogate the memory B cell Ig repertoires from two rhesus macaques after five seria
66 matic hypermutation (SHM) patterns in B cell Ig sequences have important basic science and clinical a
67 ons of activating members of the killer cell Ig-like receptor (KIR) family are not fully understood,
70 Human NK cells carry inhibitory killer cell Ig-like receptors (KIRs), which recognize distinct HLAs.
71 ng the Bw4 epitope recognized by killer cell Ig-like receptors of NK cells, allotypes having the C1 e
72 arkers c-kit and IL-7Ralpha, nor killer cell Ig-like receptors or other late-differentiation markers.
73 he C1 epitope also recognized by killer cell Ig-like receptors, and allotypes having neither epitope.
76 CTL-associated protein 4 (CTLA4), and T cell Ig and mucin domain protein-3 (TIM-3) coinhibitory signa
79 udy, we identified elevated levels of T cell Ig and mucin-domain containing molecule-3 (Tim-3)-expres
82 used on Programmed Death 1 (PD-1) and T cell Ig- and mucin-domain molecule 3 (Tim-3), which are poten
83 wer levels of the inhibitory receptor T-cell Ig and ITIM domain (TIGIT), which results in resistance
86 the frequency of CD4(+) and CD8(+) T cells, Ig(+) B cells, CD11b(+) myeloid-derived cells, and major
90 In contrast to CD80/86 antagonists (CTLA4-Ig), FR104 selectively blunts CD28 costimulation while s
93 utophagosome formation, while DCs from CTLA4-Ig-treated rheumatoid arthritis patients displayed dimin
94 e presentation of chronic rejection in CTLA4-Ig-treated LysM(C)(re) Traf6 (fl/fl) mice was similar to
96 - and stability-engineered variants of CTLA4-Ig fusion molecules with enhanced pharmacokinetic profil
99 the T cell costimulatory signal by the CTLA4-Ig synthetic protein (abatacept) could prevent SEB-depen
100 l of T cell-dependent Ab response, the CTLA4-Ig variant MEDI5265 could be formulated at >100 mg/ml fo
103 so, blocking antigen presentation with CTLA4-Ig improves RBP4-induced insulin resistance and macropha
104 ysM(C)(re) Mtor(fl/fl) recipients with CTLA4-Ig induced long-term allograft survival (>100 days) with
105 TLA4 deficiency sharply decreased with CTLA4-Ig therapy in parallel with other markers of immune dysr
107 entation by treating RBP4-Ox mice with CTLA4-Ig, which blocks costimulation of T cells, is sufficient
108 tion of activated B cells and their cytokine/Ig production in vitro, and that pharmaceutically or gen
110 nced multiple myeloma cell growth, decreased Ig light chain and HSPA5/BIP expression, activated ERK a
111 tus and is a good marker for differentiating Ig-mutated and Ig-unmutated CLL and serve as prognostic
112 nflammation and that GF mice have a distinct Ig repertoire and B cell activity, we aimed to evaluate
117 ystemic administration of the bispecific DVD-Ig or the TGF-beta mAb (1-10 mg/kg) but not the FnEDA mA
118 ction of the bispecific TGF-beta + FnEDA DVD-Ig or an FnEDA mAb, chemiluminescent detection and imagi
120 s) represent a multigene family that encodes Ig superfamily proteins that mediate activating or inhib
121 t led to heightened expression of endogenous Ig H and L chains in splenic B cells, upregulation of RA
122 ich B cells develop can affect the expressed Ig repertoire by exerting influences on the distribution
126 (DSBs) serve as obligatory intermediates for Ig heavy chain (Igh) class switch recombination (CSR).
127 ating receptor FcgammaRIII was necessary for Ig-mediated acquisition of Ags by isolated intestinal eo
128 lebsiella pneumoniae Transferring serum from Ig-deficient mice to GF animals did not alter their resp
130 ertions, whereas residues adjacent to the gD Ig-like V-type core tolerated shorter insertions (up to
131 and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using E
133 sion at the C-terminal end of the IgM heavy (Ig-mu) chains, termed the tailpiece, is necessary and su
135 d PCs with limited ER stress supporting high Ig secretion, but with a cost in terms of antigen-indepe
136 ac239, bound to and was neutralized by huCD4-Ig and rhCD4-Ig with nearly identical efficiencies.
137 ficiently neutralized by human CD4-Ig (huCD4-Ig) than by the same molecule bearing rhesus CD4 domains
140 Neuraminidase treatment of coated CHIR-human Ig proteins reduced binding of trimeric H5 proteins to C
141 ablast expansions and increased VH3 idiotype Ig; however, the mechanisms for staphylococcal modificat
145 eucine-rich repeat (LRR) and immunoglobulin (Ig) domains of Gpr124, and weakening this interaction by
146 ated by germline encoded and immunoglobulin (Ig) heavy-chain complementarity determining region 3 (HC
147 or necrosis factor (TNF) and immunoglobulin (Ig) superfamilies with diverse, and often opposing, outc
148 quantitative PCR (qPCR), and immunoglobulin (Ig)M trypomastigote excreted-secreted antigen (TESA)-blo
149 en manifests systemically as immunoglobulin (Ig)-related syndromes due to aberrant B-cell functions.
150 ollment were tested for DENV immunoglobulin (Ig) G and IgM to estimate incidence during the study per
151 interfaces of two different immunoglobulin (Ig) constant domain pairs are exchanged in part or fully
152 mmunity from OMVs comes from immunoglobulin (Ig), particularly IgG, in the milk of mucosally immunize
156 eptor repertoire analysis of immunoglobulin (Ig) and T-cell receptor (TR) rearrangements, using next-
157 ntibody titer and avidity of immunoglobulin (Ig) G specific for diphtheria toxin, pertussis toxin, fi
160 For groups 1 and 2, plasma immunoglobulin (Ig) G, IgA, and neutralizing antibody responses at week
163 f pollen) to determine serum immunoglobulin (Ig) E concentrations and Treg percentages.The probiotic
165 fection elicited significant immunoglobulin (Ig)G and IgM antibody responses, indicating bacterial co
166 mbrane protein with a single immunoglobulin (Ig) domain, instructs the distinct, neuron-type-specific
167 LPS- and flagellin-specific immunoglobulin (Ig) concentrations were associated with poor growth in y
168 dical interview and specific immunoglobulin (Ig) E levels, and he consequently underwent an oral food
171 mutator enzyme that targets immunoglobulin (Ig) genes to initiate antibody somatic hypermutation (SH
172 nected to a carboxy-terminal immunoglobulin (Ig)-like domain through a beta-hairpin stabilized by dis
173 -switch recombination of the immunoglobulin (Ig) genes occur in germinal center (GC) B cells and are
177 BPB, and MYC and upregulated immunoglobulin (Ig) light chain and HSPA5/BIP Furthermore, pathway analy
183 alternative pathway activation is similar in Ig-MPGN and C3G, suggesting similar pathogenic mechanism
189 ribution of other NK receptors (i.e., killer Ig-like receptor, LILRB1, or CD57) supported a sequentia
190 ptors, including NKG2A and inhibitory killer Ig-like receptors (KIRs), was negatively correlated with
191 TCL, except for the KIR family member killer Ig-like receptor 2DL4 (KIR2DL4; alias CD158D), which was
197 y was achieved by treating mice with LTbetaR-Ig, a therapeutic intervention currently being tested in
201 red by the difficulty in identifying mutated Ig sequences in vivo in the absence of selection pressur
202 chain variable (IgVH) region may be mutated (Ig-mutated CLL) or unmutated (Ig-unmutated CLL); and the
205 tion and induction of bnAbs, and discuss new Ig KI methodologies to manipulate the production and/or
206 nal and nonclonal mutations arise within non-Ig AID target genes in the combined absence of UNG and M
207 ive analysis of productive and nonproductive Ig gene rearrangements from transgenic mice engineered t
210 ing (NGS) technologies, a deeper analysis of Ig and/or TCR (IG/TR) gene rearrangements is now within
211 ted by polymerase chain reaction analysis of Ig/TCR gene rearrangements, and patients were assigned t
212 isplayed unique features in the third CDR of Ig H chains with minor alterations along the immunizatio
215 ing DeltaV-kappaLCs synthesize low levels of Ig and are mostly found among short-lived plasmablasts.
219 bination, however, sequential positioning of Ig loci away from the nuclear periphery determines stage
222 n in Rag2:mCherry(+) cells and the timing of Ig H and L chain expression revealed simultaneous expres
224 The influence of ovalbumin structure on Ig production upon sensitization and elicitation potency
227 ndent and T-dependent mechanisms orchestrate Ig alpha class switching and SIgA responses against comm
233 exons from gene segments generates preimmune Ig repertoires, expressed as B cell receptors (BCRs).
236 ing based on immunoglobulin/T-cell receptor (Ig/TCR) gene rearrangements and with quantification of I
238 nowledge afforded by analyses of recombinant Ig-based bnAb structures, it became apparent that key fu
242 ngabey CD4 orthologs, largely restored rhCD4-Ig neutralization of SIVmac239 and other SIV isolates.
243 ally interacts predominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (P
244 hils were unable to acquire Ag in sensitized Ig-deficient mice, and passive immunization with immune
246 d functional convergence of the SOSIP-sorted Ig repertoire, with predominant VH4 or VH5 gene family u
248 elated with the quantity of EBOV GP-specific Ig produced but not with the production of neutralizing
249 (IgCAM) BT-IgSF (brain- and testis-specific Ig superfamily protein) plays a major role in male ferti
253 t for paracellular water permeation and that Ig-like domain containing receptor 1 (ILDR1) regulates i
259 Class-switch recombination (CSR) alters the Ig isotype to diversify antibody effector functions.
262 , we demonstrate that cross-talk between the Ig-superfamily receptor CD300f and IL-5 is a key checkpo
264 ngly inhibited by the splice insert B in the Ig domain region of LAR-RPTPs, and mediate SALM5-depende
265 cterized costimulatory pathways includes the Ig superfamily members CD28 and CTLA-4 and their ligands
266 espite a common recombination machinery, the Ig heavy and Ig light chain loci rearrange in a stepwise
268 oducts (RAGE) is a scavenger receptor of the Ig family that binds damage-associated molecular pattern
269 located at the most distal 3' region of the Ig H chain locus, has multiple regulatory functions that
271 15 days postinfection, and isotyping of the Ig subclass showed that the total IgG response switched
272 anobodies against complement receptor of the Ig superfamily (CRIg), found on tissue macrophages such
274 udy shows that neuroplastin, a member of the Ig superfamily, which has previously been linked to the
281 expression occurred upon differentiation to Ig secretion, as detected by alteration from membrane to
282 intrinsic toxic effects in PCs unrelated to Ig assembly, but mediated by ER stress-associated apopto
285 rce measurements to reveal how the first two Ig-like domains of cMyPB-C (C0 and C1) interact with the
287 rra and Jin (2016) characterize a small, two-Ig domain protein, ZIG-10, and its role in maintaining s
289 ay be mutated (Ig-mutated CLL) or unmutated (Ig-unmutated CLL); and the presence or absence of mutati
295 -/-) progenitor-B cells to determine whether Ig locus contraction or nuclear positioning is decisive
297 CD79a and CD79b proteins associate with Ig receptors as integral signaling components of the B c
300 sicians to distinguish between patients with Ig-unmutated CLL, where typically have more indolent dis
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