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Memory T cells are characterized by expression of the CD45RO isoform [36], but a fraction of memory cells express CD45RA [38], [38].
Naïve cells express the high molecular weight CD45RA and activated and memory cells express the low molecular weight CD45RO [11].
Our data indicate that isolated memory cells express high levels of the RING finger protein BMI1 when compared to effector cells.
We considered SDF-1 a candidate because central memory cells express its receptor, CXCR4, and SDF-1 is expressed in bone marrow.
For normal B cell development CD27 (TNFRSF7) can be used as a marker of maturity: Naïve B cells lack it, activated B and memory cells express it moderately and plasma cells express it strongly.
A variable fraction of CD27+ memory cells express only surface IgM (IgM-only memory) and may represent pre-SM cells that will eventually join the pool of isotype SM cells after participating in subsequent germinal center reactions [ 9, 11].
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Interestingly, most of SARS-CoV S-specific memory CD4+ T cells were central memory cells expressing CD45RO+ CD45RO+D62L−.
Memory cells expressed higher protein levels of kinases that are known to play critical roles in T cell activation, including LYN, SYK, BTK and TBK1.
Some synovial, but not blood, CD8CD45RA+ memory cells expressed CCR7, which could be induced by culture in rheumatoid synovial fluid (SF).
TCRVγ9Vδ2+ T cells stimulated in the presence of growth factors and cytokines can produce abundant amounts of the pro-inflammatory cytokines and change their phenotype from memory cells expressing CCR7+ to CCR5+ expressing cells [ 6].
It has been reported that memory T cells express high levels IL-18 receptor (IL-18R) on memory T cells, and that IL-18 can induce bystander proliferation of memory phenotype CD8+ T cells [24] [26].
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