الفهرس 
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Abstract
Leprosy (also known as Hansen‟s disease) is an infection caused by bacteria called M.
leprae. These bacteria grow very slowly and it may take up to 20 years to develop signs of
the infection. Contrary to popular belief, it is not highly contagious. The two main types of
disease are based on the number of bacteria present: paucibacillary and multibacillary.
The disease can affect the nerves, skin, eyes, and lining of the nose (nasal mucosa).
The bacteria attack the nerves, which can become swollen under the skin. This can cause the
affected areas to lose the ability to sense touch and pain, which can lead to injuries, like cuts
and burns.
If left untreated, the nerve damage in leprosy patients can result in paralysis of hands
and feet. In very advanced cases, the person may have multiple injuries due to lack of
sensation, and eventually the body may reabsorb the affected digits over time, resulting in
the apparent loss of toes and fingers. Corneal ulcers and blindness can also occur if facial
nerves are affected. Early diagnosis and treatment usually prevent disability that can result
from the disease.
Interleukin -17A plays a vital role in protecting the host from infection, including
intracellular bacterial infections. IL-17A is a protein that in humans is encoded by the IL-
17A gene. It is a pro-inflammatory cytokine. it is known to be secreted by a variety of
innate cells including macrophages, DC, NK, lymphoid tissue inducer and γδ-T cells.
Interleukin-17A acts on structural cells such as epithelial cells, fibroblasts and
keratinocytes in various tissues including skin. These cells express IL-17 receptor and
produce inflammatory cytokines such as G-CSF and IL-6 as well as chemokines to attract
neutrophils and macrophages to the inflamed tissues. These inflammatory cells (neutrophils
and macrophages) can both clear the infection and initiate pathogenic inflammation.
The current study aimed to investigate the possible role of IL-17A in leprosy
pathogenesis, through analysis IL-17A (rs2275913) gene polymorphisms and IL-17A serum
levels in leprosy patients, and correlate the detected results with different clinical aspects of
leprosy in the investigated patients.
To elucidate our aim we investigated 60 patients with leprosy, and 29 age and sex
matched healthy volunteers, who have no past or family history of leprosy (control group).