Systemic Lupus Erythematosus-like Syndrome

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Normally, the immune system fights and eliminates the infectious pathogens and bacteria to keep the body healthy. An autoimmune disease is a case that the immune system attacks the host cells as it confuses the host cells for invaders. There are plenty of autoimmune diseases. Systemic lupus erythematosus (SLE) is just one of such types.

Systemic Lupus Erythematosus(SLE)

SLE is a chronic disease that has phases of worsening symptoms that alternate with periods of mild symptoms. Symptoms vary between people and can change over time. Common symptoms include severe fatigue, joint pain, joint swollen of lymph nodes, headaches, low-grade fever, butterfly rash on the face, hair loss, anemia, blooding-clotting problems, finger turning white or blue and tingling when the day gets cold. Other symptoms depend on which part of the body the disease attacks, such as the digestive tract or the heart. Digestive problems seem common in SLE. The symptoms patients may experience include nausea, diarrhea, vomiting or constipation. For the patients whose hearts are attacked by SLE, their anatomical heart structures would be affected.

Fig. 1 The illustration of systemic lupus erythematosus. (Häggström, 2014)

Fig. 1 The illustration of systemic lupus erythematosus.1

Cause of SLE

The reason for the occurrence of SLE is not clear yet. However, it is believed to involve several factors.

  1. Genetics

Genetic deficiencies in components derived from the complement system such as C1q, C2, or C4 are well known to predispose to the development of SLE. Patients with homozygous C1q deficiency develop autoantibodies and a lupus-like syndrome because of the inability to clear away apoptotic cells effectively, which leads to an increase in the exposure of antigens to the immune system. In addition, 28 more disease susceptibility loci have already been identified by genome-wide association studies. The strongest associated risk loci found in the study is ITGAM, FcγR, PRDM1-ATG5, and TNFAIP3. These newly found loci may translate into novel therapeutic targets.

  1. Environmental Factors

Ultraviolet ray is the most characterized environmental factor that triggers SLE. Both ultraviolet A 2 and ultraviolet B exposure could worsen skin diseases in patients with the disorder. Pathologically, the impact of ultraviolet B on inducing apoptotic pathway is dose-dependent and is associated with lupus autoantigen release and cytokine production. Other environmental factors that trigger SLE include certain medications, viruses, physical or emotional stress, and trauma.

  1. Sex and Hormones

SLE has a marked female predominance, with a 9:1 female to male ratio, which means that SLE affects women more than men, especially young women. Although it has not been fully proven, the gender bias is all due to oestrogen. Female patients with SLE may experience more severe symptoms during pregnancy and with their menstrual periods. These observations have led some medical professionals to believe that the female hormone estrogen may play a role in causing SLE.

Treatment for SLE

So far, there is no guaranteed cure for SLE. The goal of all the treatments is trying to ease symptoms. Treatment can vary depending on how severe your symptoms are and which part of your body SLE affects. The treatments may include anti-inflammatory medications for joint pain and stiffness, steroid creams for rashes, antimalarial drugs for skin and joint problems, disease-modifying drugs or targeted immune system agents for more severe cases.

Creative Biolabs has established advanced Complement Therapeutics Platform including antibody engineering platform, protease inhibitor platform, and drug discovery platform, and is equipped to offer a full range of biotherapeutics development services regarding drug discovery and validation for SLE. If you are interested in our services, please contact us for detailed information.

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Reference
1. Haggstrom, Mikael. "Medical gallery of mikael haggstrom 2014." WikiJournal of Medicine 1.2 (2014): 1-53.

Questions & Answer

A: Experimental research has shown that SLE-like Syndrome often presents with elevated complement activation products, such as C3a and C5a, as well as the deposition of complement components on affected tissues. Animal models and in vitro studies have been used to demonstrate the link between complement dysregulation and disease development.

A: Experimental research has identified various complement targets, including C1q, C5, and C5a receptors. Inhibition of these targets has shown promise in preclinical studies, reducing disease severity and tissue damage.

A: Future research may focus on identifying more specific complement targets, developing novel inhibitors, and refining personalized treatment approaches. Understanding the interplay between complement and other immune pathways is also a promising avenue for investigation.

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