Fig 3 - available via license: Creative Commons Attribution 4.0 International
Content may be subject to copyright.
Letter of Claude Paoletti to Jacques Monod in 1969 about the PhD defense of Gérard Orth and the response of Jacques Monod (Pasteur Institute, (MON.COR.12))
Context in source publication
Context 1
... the tumor enzyme was probably carried by the rabbit genome [9]. These results, in opposition to those of Rogers, would have allowed Gérard to defend his thesis within a reasonable time frame. However, he did not defend his PhD, despite an agreement between Jacques Monod and Claude Paoletti. Jacques Monod had agreed to be a member of the PhD jury (Fig. ...
Similar publications
Citations
... Genetic diagnosis was facilitated by using a gene list for IEIs developed by the Expert Committee of the International Union of Immunological Societies (IUIS). β-HPVs were amplified from DNA extracted from the lesion swab, as previously described [12]. Sanger sequencing was used to confirm the genotypes of β-HPVs and the STK4 variant. ...
The clinical penetrance of infectious diseases varies considerably among patients with inborn errors of immunity (IEI), even for identical genetic defects. This variability is influenced by pathogen exposure, healthcare access and host-environment interactions. We describe here a patient in his thirties who presented with epidermodysplasia verruciformis (EV) due to infection with a weakly virulent beta-papillomavirus (HPV38) and CD4 ⁺ T-cell lymphopenia. The patient was born to consanguineous parents living in the United States. Exome sequencing identified a previously unknown biallelic STK4 stop-gain mutation (p.Trp425X). The patient had no relevant history of infectious disease during childhood other than mild wart-like lesion on the skin, but he developed diffuse large B-cell lymphoma (DLBCL) and EBV viremia with a low viral load in his thirties. Despite his low CD4 ⁺ T-cell count, the patient had normal counts of CD3 ⁺ cells, predominantly double-negative T cells (67.4%), which turned out to be Vδ2 ⁺ γδ T cells. γδ T-cell expansion has frequently been observed in the 33 reported cases with STK4 deficiency. The Vδ2 γδ T cells of this STK4-deficient patient are mostly CD45RA ⁻ CD27 ⁺ CCR7 ⁺ central memory γδT cells, and their ability to proliferate in response to T-cell activation was impaired, as was that of CD4 ⁺ T cells. In conclusion, γδ T-cell expansion may act as a compensatory mechanism to combat viral infection, providing immune protection in immunocompromised individuals.
