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We propose that only a small subset of memory B cells is activated as plasmablasts during repeat infection and that plasmablast responses are not representative of the memory B cell repertoire after dengue infection.
We identify a core transcriptional profile within the CD69+ subset of memory CD4+ and CD8+ T cells in lung and spleen that is distinct from that of CD69− TEM cells in tissues and circulation and defines human TRMs based on homology to the transcriptional profile of mouse CD8+ TRMs.
We measured a reduction of the CD27+ subset of memory B cells in patients with both metastatic and non-metastatic melanoma compared to healthy volunteers (Figure S2).
It is known that a subset of memory CD4+ T cells in normal individuals also express CD45RA and that a second marker, such as CD62L needs to be used to exclude this subset from the naïve pool [24].
This could be advantageous for scaffolding or other structure-guided immunogen approaches where, perhaps, a less fixed conformation could first prime a B cell response, and then, a more conformationally fixed, and superior structural mimetic, might drive the desired subset of memory B cells to a desired epitope.
Among CD4+ T cells, we observed that a subset of memory cells displayed low levels of SAMHD1 (Fig. 2a).
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Additional studies have attempted selectively expanding different subsets of memory T cells, using different methods to expand cells, or transducing cells to express HIV-1 specific TCR chains [26] [28].
Broadly, two subsets of memory CD8+ T cells are described: central memory CD8+ T cells (TCM) and the effector memory CD8+ T cells (TEM) (Sallusto et al., 1999).
Moreover, subsets of memory PCs may reside in alternative niches [ 14, 15], which might be differently modified by therapeutic treatments [ 16].
In the circulation it is also expressed by discrete subsets of memory CD4+ and CD8+ lymphocytes expressing the intestinal homing receptor α4β7 [ 15].
HIV infection has been associated with a wide range of B-cell defects, including decreased B-cell survival [ 17], enhanced expression of markers of B-cell activation, reduction of subsets of memory B-cells, polyclonal hypergammaglobulinemia, and impaired antibody responses to immunizations, for example S. pneumoniae[ 18- 25].
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