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1 ability of this mutant strain to bind human immunoglobulin D.
2 ells stimulated with dextran-conjugated anti-immunoglobulin D (anti-IgD) antibodies (anti-Ig-dex), a
3 1/GFP knock-in mice could be subdivided, and immunoglobulin D(H)-J(H) rearrangements, as well as tran
8 esponse; after immunization with antibody to immunoglobulin D (IgD), CD1-deficient mice produced IgE.
9 uency of gammaHV68 infection was observed in immunoglobulin D (IgD)-negative B cells, which was stabl
10 ation of cells characterized as CD19(hi) and immunoglobulin D negative, a phenotype that is consisten
11 rus was able to establish latency in surface immunoglobulin D-negative (sIgD(-)) B cells; by 6 months
13 receptor associated periodic syndrome; hyper immunoglobulin D syndrome; neonatal onset multisystemic
14 on of CD22, Fcgamma receptor IIb, CD79b, and immunoglobulin D that are down-regulated by cell trigger
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