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On the one hand, defects in the complement system might cause a deficient presentation of antigens in the bone marrow and diminish the protection of the receptor editing mechanism.
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Our data support the notion that susceptibility of Batf3 −/− mice to L. major infection is not caused by deficient antigen presentation.
Only one G6PD deficient patient presented.
In contrast with TAP-independent Lass5 epitope presentation, TAP-deficient tumor cells were unable to present the TAP-dependent and Db-restricted NP366 374 epitope when cells were infected with VV carrying the NP366 374 minigene (Fig.4 B right).
In contrast, numbers of CD8α+ conventional DCs (cDCs) in skin-dLNs are not significantly affected by Batf3 deficiency in the C57BL/6 background, although they are partially impaired in function, for example CD8α+ cDCs show deficient cell-associated cross-presentation [ 11– 13].
A comparison of patient and tumour characteristics between patients with intact MMR and patients with deficient MMR is presented in Table 4. Patients with deficient MMR tended to be younger and had a lower frequency of distant metastasis at presentation.
$$\end{document} Here, peptide-pulsed T2 cells, a transporter associated with antigen presentation-deficient HLA-A*0201+ HLA-A*0201+AmericellType Celineollection (AmericanRL-No.: 1992, Rockville, MD, USA), were used as Typeet Cells.
Despite differences in disease presentation in CCR-deficient mice, there was no significant difference in viral load.
Another possible mechanism for failure of intranasal tolerance induction in complement-deficient mice could involve antigen presentation per se.
24, 25 The striking discrepancy between an expected moderate impairment of mitochondrial fatty acid oxidation and the severe clinical presentation of ECHS1-deficient individuals argues for an additional pathomechanism.
The less effective induction of ICOS and PD1 on T cells responding to SRBC-Ova in EBI2-deficient hosts suggests that antigen presentation by CD4+ DCs may be important in favoring induction of an early B-helper phenotype in CD4 T cells.
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