scholarly journals Severe Cellular Immunodeficiency Triggered by the CDK4/6 Inhibitor Palbociclib

2020 ◽  
Vol 20 (2) ◽  
pp. e192-e195 ◽  
Author(s):  
Zoé Guillaume ◽  
Jacques Medioni ◽  
Agnes Lillo-Lelouet ◽  
Grégoire Marret ◽  
Stéphane Oudard ◽  
...  
2008 ◽  
Vol 79 (1) ◽  
pp. 1-6 ◽  
Author(s):  
J. PRIETO ◽  
M. L. SUBIRÁ ◽  
A. CASTILLA ◽  
M. P. CIVEIRA ◽  
M. SERRANO

Blood ◽  
1982 ◽  
Vol 60 (4) ◽  
pp. 814-821 ◽  
Author(s):  
S Ladisch ◽  
W Ho ◽  
D Matheson ◽  
R Pilkington ◽  
G Hartman

Depressed cellular immune function and increased susceptibility to infection characterize familial erythrophagocytic lymphohistiocytosis (FEL), a usually fatal autosomal recessive disease. One component of the immunodeficiency is plasma-mediated inhibition of lymphocyte proliferation. We have tested whether repeated plasma or blood exchange would decrease plasma inhibitory activity and improve cellular immune function in FEL. Following this treatment, reduction in plasma inhibitory activity, reversal of depressed antigen-specific lymphocyte proliferative responses and monocyte antibody-dependent cytotoxic function in vitro, and clinical improvement were complete in two and partial in one of three patients studied. Relapse, which was ultimately fatal, was associated with recurrence of the immune defects. These findings suggest that cellular immunodeficiency in FEL is acquired and possibly related to circulating immunosuppressive activity, the removal of which is associated with transient immunologic and clinical recovery.


Author(s):  
Sami Khalife ◽  
Jocelyn Soffer

Since 1981, when previously healthy young adults were first stricken with a mysterious illness that was eventually described as “a new acquired cellular immunodeficiency” (Gottlieb et al., 1981), understanding of HIV and AIDS, both the in the medical community and general society, has come a long way. There remains, however, an unfortunate degree of stigma that persists since its development in the early days of the illness (Cohen and Weisman, 1986; Cohen, 1987, 1992; Cohen and Alfonso, 1998;Cohen, 2008). Early in the course of this epidemic, as it became evident that the immune deficiency had an infectious etiology and could lead to rapidly fatal complications, many became fearful of the possibility of contagion. An “epidemic of fear” (Hunter, 1990) thus began to develop along with the AIDS epidemic. During the first decade, even many physicians surveyed had negative attitudes toward persons with HIV and AIDS (Kelly et al., 1987; Thompson, 1987; Wormser and Joline, 1989). At the beginning of the HIV epidemic some persons hospitalized with AIDS experienced difficulty receiving even minimally adequate care, including getting their rooms cleaned, obtaining water or food, and receiving proper medical attention. Psychiatric consultations for AIDS patients with depression, withdrawal, and treatment refusal often revealed the heightened feelings of isolation and depression experienced by the patients, in part as a result of the reactions of staff members to their illness, including the palpable fear of contagion. Holtz and coauthors (1983) were the first to describe the profound withdrawal from human contact as the “sheet sign,” observed when persons with AIDS hid under their sheets and completely covered their faces. Thus, since the beginning of the AIDS epidemic, people with AIDS have been stigmatized. They have felt shunned and ostracized by not only medical caregivers but also the general community and even by their own families and friends. In some areas of the world, persons with AIDS have been quarantined because of the irrational fears, discrimination, and stigma associated with this pandemic. In the United States, persons with AIDS have lost their homes and jobs, and some children and adolescents have been excluded from classrooms.


1994 ◽  
Vol 57 (6) ◽  
pp. 836-840 ◽  
Author(s):  
Karl Ulrich Petry ◽  
Danicla Scheffel ◽  
Ulrike Bode ◽  
Thomas Gabrysiak ◽  
Heinrich Köchel ◽  
...  

1979 ◽  
Vol 132 (1) ◽  
pp. 43-48 ◽  
Author(s):  
D. Niethammer ◽  
S. F. Goldmann ◽  
H. -D. Flad ◽  
W. Meigel ◽  
U. T�llner ◽  
...  

1977 ◽  
Vol 296 (12) ◽  
pp. 651-655 ◽  
Author(s):  
J. W. Stoop ◽  
B. J. M. Zegers ◽  
G. F. M. Hendrickx ◽  
L. H. Siegenbeek van Heukelom ◽  
G. E. J. Staal ◽  
...  

Blood ◽  
2001 ◽  
Vol 97 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Elie Haddad ◽  
José L. Zugaza ◽  
Fawzia Louache ◽  
Najet Debili ◽  
Catherine Crouin ◽  
...  

Abstract In studies aimed at further characterizing the cellular immunodeficiency of the Wiskott-Aldrich syndrome (WAS), we found that T lymphocytes from WAS patients display abnormal chemotaxis in response to the T-cell chemoattractant stromal cell–derived factor (SDF)-1. The Wiskott- Aldrich syndrome protein (WASP), together with the Rho family GTPase Cdc42, control stimulus-induced actin cytoskeleton rearrangements that are involved in cell motility. Because WASP is an effector of Cdc42, we further studied how Cdc42 and WASP are involved in SDF-1–induced chemotaxis of T lymphocytes. We provide here direct evidence that SDF-1 activates Cdc42. We then specifically investigated the role of the interaction between Cdc42 and WASP in SDF-1–responsive cells. This was achieved by abrogating this interaction with a recombinant polypeptide (TAT-CRIB), comprising the Cdc42/Rac interactive binding (CRIB) domain of WASP and a human immunodeficiency virus–TAT peptide that renders the fusion protein cell-permeant. This TAT-CRIB protein was shown to bind specifically to Cdc42-GTP and to inhibit the chemotactic response of a T-cell line to SDF-1. Altogether, these data demonstrate that Cdc42-WASP interaction is critical for SDF-1–induced chemotaxis of T cells.


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