Although many of these models are deficient in functions related to lymphocytes or clearance of apoptotic cells, there are others in which there is no apparent rationale for the development of a lupus-like disease.
The fact that cytosolic iron depletion occurs in conjunction with mitochondrial iron overload may explain why cytosolic iron−sulfur proteins have been known to be deficient in function.
These cells are deficient in ept function and Psn activity, but give rise to easily detectable clones due to their inability to die.
Interestingly, it has been demonstrated that whereas circulating DCs isolated from patients with cancer are deficient in their function, DCs conditioned in vitro in the absence of tumor products have the capacity to induce robust immune responses [ 9, 10].
In addition, we determined whether a specific methyl-CpG binding protein, MeCP2, is necessary for the inactive X histone modification pattern by studying Rett syndrome cells which are deficient in MeCP2 function.
Because wild-type λ-phage DNA replicate poorly in the presence of P2 lysogens in the host cells (called "sensitive to P2 interference" or "Spi"), only mutant λ phages that are deficient in the functions of both the redBA and gam genes are able to escape from P2 interference (called "Spi−") and form visible clear plaques on a bacterial lawn.
Thus, it is possible that the variant could produce a dominant-negative mutant that efficiently binds wild-type DLC1 monomers to form heterodimers that are deficient in its own function but amplifies the effect of CDK6, i.e., protective when CDK6 functions normally and risky when CDK6 is mutated.
Recent studies have demonstrated that acute lymphoblastic leukemia-derived pre-B cell lines are deficient in their costimulatory function for T cell proliferation in response to the mitogen Con A and the superantigens TSST-1 and SEB.
Previous studies have shown that NOD mice are deficient in Treg number and function [35] [37] and that intravenous transfer of β cell-specific ex vivo expanded Tregs into NOD mice actively prevents diabetes [38], [39].
There is evidence suggesting that atopic individuals are deficient in regulatory T cells whose function is specifically to depress the B cells that produce IgE and that desensitization treatment may overcome this deficiency.
Cells or animals lacking DNA-PK functions are deficient in a protective response to ionizing radiation and various radiomimetic agents [10], [11].
