NCT05093257

Study of T Cells and Natural Killer Cells Expression in Patients With Immune Thrombocytopenic Purpura

• Status: Unknown
• Phase: —
• Study type: Observational
• Enrollment: 40 (estimated)
• Sponsor: Sohag University · Academic / Other
• Sex: All
• Age: 1 Year – 50 Years
• Healthy volunteers: Accepted

Summary

Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by bleeding due to isolated thrombocytopenia with platelet count less than 100 × 109/L. ITP is classified based on course of disease into acute (3- \<12 months), and chronic (≥12 months). ITP usually has a chronic course in adults whereas approximately 80-90% of children undergo spontaneous remission within weeks to months of disease onset. The main pathogenesis of ITP is the loss of immune tolerance to platelet auto-antigens, which results in increased platelet destruction and impaired thrombopoiesis by autoantibodies and cytotoxic T lymphocytes (CTLs). Platelet autoantibodies, particularly antiglycoprotein (GP) GPIIbIIIa and anti-GPIbIX, are known to cause thrombocytopenia in patients with ITP. As a main component of cellular immunity, T cells play an important role in body defense and peripheral tolerance. Changing number and function of these cells is closely associated with various diseases, including ITP.NK cells can also modulate cellular immunity in ITP patients.

Detailed description

Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by bleeding due to isolated thrombocytopenia with platelet count less than 100 × 109/L.ITP is classified based on course of disease into acute (3- \<12 months), and chronic (≥12 months). ITP usually has a chronic course in adults whereas approximately 80-90% of children undergo spontaneous remission within weeks to months of disease onset. The main pathogenesis of ITP is the loss of immune tolerance to platelet auto-antigens, which results in increased platelet destruction and impaired thrombopoiesis by autoantibodies and cytotoxic T lymphocytes (CTLs).Platelet autoantibodies, particularly antiglycoprotein (GP) GPIIbIIIa and anti-GPIbIX, are known to cause thrombocytopenia in patients with ITP. Auto-Abs production often occurs due to the loss of self-tolerance and increased stimulation of the immune system. The immune system includes a variety of B- and T cells which cooperate with each other in T-cell-dependent antibody production reactions and play significant roles in humoral and cellular immunity. Although the pathogenesis of ITP has not been clearly understood, the autoreactive B- and T cells have been directly and indirectly involved in Auto-Abs production, respectively. As a main component of cellular immunity, T cells play an important role in body defense and peripheral tolerance. Changing number and function of these cells is closely associated with various diseases, including ITP. It can be stated that CD4+ T cells are indirectly involved in ITP pathogenesis by inducing the increased activity of B cells during Auto-Abs production. Cytotoxic T lymphocytes (CTLs) are another subgroup of T lymphocytes characterized by the expression of CD8+ surface marker, destroying the pathogenic factors via granzyme and perforin production. These cells are increased in ITP patients and are involved in platelet destruction via augmented production of granzyme and perforin. NK cells can also modulate cellular immunity in ITP patients.

Conditions

• Immune Thrombocytopenic Purpura

Interventions

Type	Name	Description
DIAGNOSTIC_TEST	Laboratory investigations for control	1. Complete blood picture . 2. Erythrocyte sedimentation rate(ESR). 3. Liver function tests . 4. Kidney function tests. 5. CD3, CD4,CD8,CD16,CD56 from peripheral blood samples by Flowcytometry
DIAGNOSTIC_TEST	Laboratory investigations for patients	1. Complete blood picture . 2. Erythrocyte sedimentation rate(ESR). 3. Liver function tests . 4. Kidney function tests. 5. Anti-nuclear antibodies test by immunoflourescence for ITP patients. 6. Bone marrow aspiration (for diagnosis of ITP). 7. CD3, CD4,CD8,CD16,CD56 from peripheral blood samples by Flowcytometry.

Timeline

• Start date: 2021-11-01
• Primary completion: 2022-11-01
• Completion: 2022-12-01
• First posted: 2021-10-26
• Last updated: 2021-10-26