Induction and Characterization of Human Immune (Gamma) Interferon

1982 ◽  
pp. 150-158
Author(s):  
J. Vilček ◽  
Y. K. Yip ◽  
R. H. L. Pang
2021 ◽  
Author(s):  
Blanca Garcia Solis ◽  
Ana Van Den Rym ◽  
Jareb J. Pérez-Caraballo ◽  
Abdulwahab Al –Ayoubi ◽  
Lazaro Lorenzo ◽  
...  

Abstract The CARD-BCL10-MALT1 (CBM) complex is critical for the proper assembly of human immune responses. The clinical and immunological consequences of deficiencies in some of its components such as CARD9, CARD11, and MALT1 have been elucidated in detail. However, the scarcity of BCL10 deficient patients prevented gaining that knowledge for this genetic disease. Only two patients with BCL10 deficiency have been reported to date. Here we describe in more depth an additional patient with autosomal recessive BCL10 complete deficiency caused by a nonsense mutation that leads to a loss of expression (K63X). Using mass cytometry coupled with unsupervised clustering and machine learning computational methods, we obtained a thorough characterization of the consequences of BCL10 deficiency in different populations of leukocytes. We showed that in addition to the almost absence of memory B and T cells reported before, this patient display a reduction in NK, gdT, Tregs, and TFH cells. The patient suffered from recurrent respiratory infections since early in life, and showed a family history of lethal severe infectious diseases. Fortunately, hematopoietic stem-cell transplantation (HSCT) cured her. Overall, this report highlights the importance of early genetic diagnosis for the management of BCL10 deficient patients and HSCT as the recommended treatment to cured this disease.


1979 ◽  
Vol 26 (1) ◽  
pp. 36-41 ◽  
Author(s):  
M P Langford ◽  
J A Georgiades ◽  
G J Stanton ◽  
F Dianzani ◽  
H M Johnson

2005 ◽  
Vol 25 (14) ◽  
pp. 6247-6258 ◽  
Author(s):  
Huifang M. Zhang ◽  
Ji Yuan ◽  
Paul Cheung ◽  
David Chau ◽  
Brian W. Wong ◽  
...  

ABSTRACT Gamma interferon-inducible protein 10 (IP10) is a member of the CXC family of chemokines. By differential mRNA display, we have demonstrated the upregulation of IP10 in coxsackievirus B3 (CVB3)-infected mouse hearts. Functional characterization of the IP10 gene in IP10-transfected Tet-On HeLa cells has found that IP10 induced cell apoptosis and inhibited viral replication. In the characterization of the IP10-induced apoptotic pathway, we found that overexpression of IP10 upregulated p53 and resulted in altered expression of p53-responsive genes such as the p21Cip1, p27kip1, NF-κB, Bax, and PUMA genes and the mitochondrial translocation of Bax. However, transduction of the IP10 cells with adenovirus expressing dominant negative p53 not only ablated p53-triggered gene expression but also abolished IP10-induced apoptosis and restored CVB3 replication to the control levels. These data suggest a novel mechanism by which IP10 inhibits viral replication through the induction of host cell death via a p53-mediated apoptotic pathway. We also found that constantly high-level expression of p53 in these tumor cells is attributed to the IP10-induced suppression of human papillomavirus E6 and E7 oncogene expression. Taken together, these data reveal not only a previously unrecognized link between chemokine IP10 and p53 in antiviral defense but also a mechanism by which IP10 inhibits tumor cell growth.


2012 ◽  
Vol 189 (2) ◽  
pp. 935-945 ◽  
Author(s):  
Larissa N. A. Longhi ◽  
Rosiane M. da Silva ◽  
Márcia C. Fornazim ◽  
Maria C. Spago ◽  
Rômulo T. D. de Oliveira ◽  
...  

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