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Importantly, we observed complementation of immunodeficiency to Listeria by chronic herpesvirus infection in four different strains of immunodeficient mice, revealing virus infection as one possible environmental factor that might alter the genotype-phenotype relationship for patients with mutations in immune system genes.
Why present adult-onset immunodeficiency to a readership of rheumatologists?
The principal issue is: what amount of measurable phenotypic or functional cellular depression is needed in order for a clinically relevant immunodeficiency to occur.
Because of the role of immunodeficiency to viral antigens eventually leading to cancer, EV has become a model for understanding a viral role in cutaneous oncogenesis.
The immunodeficiency to L. monocytogenes was linked to problems producing protective molecules called cytokines, which form a crucial part of the immune response.
For this study, we measured EBV DNA load in pretreatment serum from 127 diffuse large B‐cell lymphoma patients without any underlying immunodeficiency to evaluate its effects on clinical manifestations and prognosis.
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Mutations in human NHEJ genes can lead to immunodeficiency due to its role in V(D J recombination in the immune system.
It is consequently concluded that RAG mutations can be responsible for clinical presentations spanning from severe immunodeficiencies to an almost normal phenotype, as seen in this patient with ICL.
This study was undertaken to evaluate a specific lymphocyte transformation assay to Cryptococcus neoformans in order to identify immunodeficiency associated to NCC as primary cause of the mycosis.
We aimed to evaluate a specific lymphocyte transformation assay to Cryptococcus neoformans in order to identify immunodeficiency associated to neurocryptococcosis (NCC) as primary cause of the mycosis.
The incidences of other events potentially suggestive of an immunodeficiency, due to either severity or due to the specific nature of the infection, were also examined.
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