الفهرس 
Aim of the workOnly 14 pages are availabe for public view
 |  | from | 150 |  |  |
| | | from | 150 | | |
Abstract
Systemic lupus erythematosus and ankylosing spondylitis are two different autoimmune diseases with distinct etiologic and pathogenic patterns. SLE is an immunological disorder with female predominance of unclear cause characterized by dysregulated interferon response and loss of cellular antigens self-tolerance causing damage to many organs in the body with alternating activity and remission. The production of ANA is the most prominent immunologic abnormality of this disease. Clinical symptoms of SLE are variable ranging from mild arthritis and skin affection to lifethreatening kidney, blood, or brain and spinal cord involvement. Due to clinical heterogeneity and the lack of pathognomonic features or tests, SLE diagnosis is considered a difficult challenge. SLE diagnosis is depending generally on clinical manifestations and laboratory data.
Ankylosing spondylitis is the one type of seronegative SpA that affects young adults and involves the articular joints and the axial skeleton. The inflammatory process also affects tendons, cartilaginous tissue, and peripheral joints and lasts for many years before causing inevitable damage. Also, uveitis and psoriasis are examples of extra-articular manifestations that could occur in this disease.
Several studies have shown that SLE and AS susceptibility is associated with a strong genetic predisposition.
Finding novel biomarkers, which could serve as prognostic or diagnostic indicators for SLE and AS are needed. The identification of such biomarkers will probably be crucial for the diagnosis, treatment, and management of these diseases. One member of the PTP family, named CD45, is encoded by PTPRC gene. It has an important role in the regulation of the signaling of antigen receptors in B and T cells, causing negative regulation of cytokine receptor signaling, and inhibition of Janus kinases. One of the members of the JAK family is the JAK2 gene, which has pivotal role in immune cell differentiation, proliferation, and survival. JAK1, JAK3, and Tyk2 are further members of this family that make up non receptor PTKs. Also, PTKs are the most crucial component of the JAK/STAT signaling pathway and dysregulation is thought to be involved in SLE progression.
As shown by knockout mice for certain JAKs, JAK mediated signaling transduction is related to surface receptors for a variety of cytokines and is crucial for bone formation and metabolism. Small medicines that target JAK, such as tofacitinib, have been utilized to treat AS since the condition is marked by severe inflammation and abnormal osteoblastic differentiation.
The aim of this work is to study the role of JAK2 and PTPRC mRNA expression in SLE and AS patients.
This present hospital-based case-control study was done on 96 subjects separated into three groups. group I included 32 Egyptian SLE patients, and group II with 32 Egyptian AS patients, these two groups recruited from rheumatology and clinical immunology outpatient clinic, the outpatient clinic of the Rheumatology, Physical Medicine, and Rehabilitation Department, in collaboration with the Biochemistry and Molecular Biology Department, in the duration between April 2021 to October 2021 with group III of 32 healthy persons matched in age and sex, considered as a control group.
Patients underwent a thorough clinical examination, a full history review, and the collection of demographic information. For AS patients, BASDAI with CRP (mg/l) and ESR (mm/h) were used to assess disease activity. BASMI and BASFI were used to assess mobility and functional limitations. In SLE group of patients, the disease activity was assessed by SLEDAI, active SLE patients have SLEDAI score ≥ 10 and the inactive SLE patients have SLEDAI score <10. mRNA analysis of JAK2 and PTPRC by Real-time PCR.