Exacerbation of Psoriasis under Efalizumab Therapy

2009 ◽  
Vol 13 (2) ◽  
pp. 106-109 ◽  
Author(s):  
Efstathios Rallis ◽  
Constantinos Verros ◽  
Evmorfia Karanikola ◽  
Argyro Valaskatzi ◽  
Markos Papaconstantis
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Adverse Events ◽  
Blood Cell ◽  
T Cell Activation ◽  
Plaque Psoriasis ◽  
Lymphocyte Count ◽  
Cell Activation ◽  
Total White Blood Cell ◽  
Blood Cell Count

Background: Efalizumab is a recombinant humanized IgG1-κ isotype monoclonal antibody that binds to CD11a, inhibiting T-cell activation. It has been approved for the treatment of moderate to severe plaque psoriasis. Efalizumab has been associated with the development of skin eruptions during the administration period, and this probably represents the potential psoriasis events observed during its administration. Objective: We report a case of exacerbation of psoriasis under efalizumab administration. A reversible increase in lymphocyte count with normal total white blood cell count was also noticed. Conclusion: Larger series are probably needed to establish clinical and histopathologic criteria and to determine the terminology used regarding the psoriasis adverse events seen with efalizumab treatment.

HUMAN T-CELL ACTIVATION IS AUGMENTED BY MONOCLONAL ANTIBODY TO IgD

1982 ◽  
Vol 399 (1 Immunoglobuli) ◽  
pp. 227-237
Author(s):  
Denis R. Burger ◽  
David Regan ◽  
Karen Williams ◽  
Gerrie Leslie
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Human T Cell

scholarly journals Decreased Cytokine Plasma Levels and Changes in T-Cell Activation Are Associated With Hemodynamic Improvement and Clinical Outcomes After Percutaneous Mitral Commissurotomy in Patients With Rheumatic Mitral Stenosis

2021 ◽  
Vol 7 ◽  
Author(s):  
Vicente R. Silva ◽  
Eula G. A. Neves ◽  
Lívia S. Araújo Passos ◽  
Flávia Cristina de Melo ◽  
Andrea Teixeira-Carvalho ◽  
...  
Keyword(s):  
T Cell ◽  
Adverse Events ◽  
Clinical Outcomes ◽  
T Cell Activation ◽  
Plasma Levels ◽  
Mitral Stenosis ◽  
Cell Activation ◽  
Hemodynamic Improvement ◽  
Mitral Commissurotomy

Mitral stenosis (MS) is a consequence of rheumatic heart disease that leads to heart failure requiring mechanical intervention. Percutaneous mitral commissurotomy (PMC) is the treatment of choice for the intervention, and currently there are no soluble markers associated with hemodynamic improvement after PMC. This study aims to determine the changes in cytokine/chemokine plasma levels, as well as T cell activation after PMC, and to investigate their association with immediate hemodynamic improvement and clinical outcomes. Plasma samples from eighteen patients with well-defined MS who underwent PMC and 12 healthy controls were analyzed using BioPlex immunoassay. We observed that 16 out of the 27 (60%) molecules assessed were altered in patients' plasma pre-PMC as compared to control group. Of those, IL-1β, IL-12, IL-6, IL-4, PDGF, and CCL11 showed significant decrease after PMC. Stratifying the patients according to adverse outcome after a 28-month median follow up, we detected a significant reduction of IL-1β, IL-12, IL-6, IL-4, IFN-γ, CXCL-10, VEGF, FGF and PDGF post-PMC in patients without events, but not in those who presented adverse events during the follow-up. Patients with adverse outcomes had lower IL-10 pre-PMC, as compared to the ones without adverse events. In addition, the frequency of CD8+ activated memory cells was increased after PMC, while the frequency of CD4+ activated memory cells did not change. Our results show an association between the decrease of specific cytokines and changes in T cell activation with hemodynamic improvement post-PMC, as well as with long-term outcomes, suggesting their possible use as soluble markers for hemodynamic recovery after MS intervention.

scholarly journals Agonist Anti-Human CD27 Monoclonal Antibody Induces T Cell Activation and Tumor Immunity in Human CD27–Transgenic Mice

2013 ◽  
Vol 191 (8) ◽  
pp. 4174-4183 ◽  
Author(s):  
Li-Zhen He ◽  
Naseem Prostak ◽  
Lawrence J. Thomas ◽  
Laura Vitale ◽  
Jeffrey Weidlick ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Transgenic Mice ◽  
Tumor Immunity ◽  
T Cell Activation ◽  
Cell Activation

scholarly journals Activation of CD4+ T cells in the presence of a nondepleting monoclonal antibody to CD4 induces a Th2-type response in vitro.

1995 ◽  
Vol 182 (1) ◽  
pp. 5-13 ◽  
Author(s):  
P Stumbles ◽  
D Mason
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Primary Cultures ◽  
In Vitro Experiments ◽  
Ifn Gamma

In vitro experiments using purified rat CD4+ T cells in primary and secondary mixed leukocyte cultures (MLC) have been carried out to explore the mechanism of inhibition of cell-mediated autoimmune disease in the rat by a nondepleting monoclonal antibody (mAb) to CD4. Previous work has shown that W3/25, a mouse anti-rat CD4 mAb of immunoglobulin G1 isotype, completely prevents the development of the paralysis associated with experimental allergic encephalomyelitis (EAE) in Lewis rats, but does so without eliminating the encephalitogenic T cells. The in vitro experiments described in this study have shown that when CD4+ T cells were activated in the presence of the anti-CD4 mAb in a primary MLC, the synthesis of interferon (IFN) gamma, but not interleukin (IL) 2, was completely inhibited. After secondary stimulation, now in the absence of the mAb, the synthesis of IL-4 and IL-13 mRNA was greatly enhanced compared with that observed from CD4+ T cells derived from primary cultures in which the mAb was omitted. As IL-4 and IL-13 are known to antagonize cell-mediated immune reactions, and as EAE is cell-mediated disease, the data suggest that the W3/25 mAb controls EAE by modifying the cytokine repertoire of T cells that respond to the encephalitogen. The capacity for the mAb to suppress IFN-gamma synthesis provides, in part, an explanation for this change in cytokine production. These findings are discussed in terms of what is known of the factors that determine which cytokine genes are expressed on T cell activation. Possible implications for the evolution of T cell responses in human immunodeficiency virus infection are also discussed.

scholarly journals An Anti-CD2 Monoclonal Antibody That Both Inhibits and Stimulates T Cell Activation Recognizes a Subregion of CD2 Distinct from Known Ligand-Binding Sites

1993 ◽  
Vol 150 (2) ◽  
pp. 235-246 ◽  
Author(s):  
Karen F. Kozarsky ◽  
Carlene Tsai ◽  
Cynthia M. Bott ◽  
Gopal Allada ◽  
Lan Lan Li ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
Ligand Binding ◽  
T Cell Activation ◽  
Binding Sites ◽  
Cell Activation ◽  
Ligand Binding Sites

Differential modulation of the CD-2 and CD-3 T cell activation pathways by a monoclonal antibody to Leu-13

1991 ◽  
Vol 132 (2) ◽  
pp. 366-376 ◽  
Author(s):  
Susan Levine ◽  
Chen Yu Xian ◽  
Bede Agocha ◽  
Janet Allopenna ◽  
Karl Welte ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Differential Modulation ◽  
Activation Pathways
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