B lymphocytes: SLE is characterized by the generation of large amounts of auto antibodies directed against variety of self-antigens, and the loss of B cell tolerance plays a key role in the disease (Ahmadpoor et al et al., 2014). Defective B cell tolerance is a hallmark of SLE; B cell tolerance is defective at several levels in SLE, both central and peripheral checkpoints that remove self-reactive B cells are defective in patients with SLE (Liu and Davidson, 2012). B-cell tolerance is developed at multiple checkpoints throughout B cell development, both in the bone marrow (BM) and the periphery. In BM, the immature B lymphocytes that recognize self antigens with high affinity, a strong BCR signal, are either passively deleted or their specificity …show more content…
These include: ptpn22 polymorphisms, and limited Fc type II receptor–mediated suppression (George and Tsokos, 2011). Peripheral selection is similarly defective in SLE, allowing auto reactive B cells further differentiate into pathogenic memory and plasma cells. This could be the result of defects in B cell signaling or death, excess of T cell help, excess of self antigens, or even impaired function of various regulatory cells, for example: B cells or T cells. Auto reactive B cells can also be expanded outside germinal centers, this result from excess inflammatory signals, such as IL-12, TLR ligation, or CD40 ligation, which preferentially promote B cell expansion in extra-follicular foci and the generation of short-lived plasma cells (Liu and Davidson, …show more content…
However, B cells can contribute to the SLE pathogenesis through additional pathways; B cells of patients with SLE have been shown to present auto-antigens to T cells and further amplify T-cell activation, regulate and organize inflammatory responses through cytokine and chemokine secretion (such as IL- 10, IL-6, interferon-γ, and lymphotoxin-α), and regulating other immune cells (Ahmadpoor et al et al.,
No one knows exactly what causes the body’s immune system to attack the beta cells, but they believe that autoimmune, genetic, and environmental factors, possibly viruses, are involved.
As I was doing my research I came across the autoimmune part and totally lost. It’s a breakdown in the immune system. As we know every person produces their own cell types that fight off disease and infection. In order to fight off the bad bacteria our bodies must be able to recognize the bad known as antigens (often proteins) on the surface of the UN wanted invaders. Everyone’s immune system should be able to recognize the bad, and be able to fight it off. In an autoimmunity this is where the immune system is not able to recognize the invaders and fight them off.
Lupus is a chronic inflammatory disease of unknown cause that can affect virtually any part of the body. The medical term for Lupus is Systemic Lupus Erythematosus or better known as SLE. With Lupus there is a malfunction in some of the cells of the immune system. "In Lupus, the body overreacts to an unknown stimulus and makes to many antibodies, or proteins directed against body tissue. Thus, Lupus is called an autoimmune disease. ”#
Both medical journals provide similar information about SLE dealing with genetic influence, hormones, cytokines and similar treatment. Only difference is Mechanisms of Disease Systemic Lupus Erythematosus gives information about environmental influence and A Review of Systemic Lupus Erythematosus and Current Treatment Options journal has no evidence to support any environmental influence. It gives details about the new medication, Belimumab, which was approved by Food and Drug Administration (FDA). The results are small but significant beneficial with the blockade of B-lymphocyte stimulator with an anti-BLyS antibody (Tsokos, 2011). Another new treatment option is small molecule inhibitors of kinases such as Syk and CaMK4 that are showed in the immune cells of patients with SLE (Tsokos,
These alien like materials are known as antigens. Having an autoimmune condition such as SLE, the body 's system may lose its ability to know the transformation among remote substances knowing as antigens and our normal cells and tissues. Our body system makes up these well-known antibodies engaged against itself. Our immune system protects our antibodies from the reaction within the body antigens to form protection and developments. The protected multiple factors build up in our tissues and can cause inflammation, injury to the normal cell, tissues, and cause pain. African American, Latino, and Asian women are more commonly affected by SLE than Caucasian women.
Makover, M. & Zieve, D. (2011, February 14). Systemic Lupus Erythematosus. National Center for Biotechnology Information. Retrieved July
To understand autoimmune diseases, the general characteristic of autoimmunity must be addressed. Autoimmunity is defined, in short, as “ misdirected immune response”. A healthy person is equipped with the mechanisms necessary to defend the body from pathogens within the immune system. When autoimmunity is present in an individual, something within the immune system is
Tissue sample presented with large population of B cells, labelled with CD20, in follicles and macrophages labelled with CD68 were also visible in the intrafollicular zone, both are indicative of a humoral immune response.
Lupus is a chronic inflammatory disease marked by its effect on various parts of the body, including the joints, skin, blood, and kidneys. It is a condition in which the body's immune system attacks its own cells and tissues, resulting in pain, inflammation, and often damage to organs. Lupus involves the immune system. The immune system makes antibodies that work to protect the body against foreign substances like viruses and bacteria. Such foreign bodies are called antigens. When a person has lupus, his or her body is unable to determine the difference between antigens and the individual's cells and body tissues. As such, the immune system creates antibodies against the individual's own tissues. These antibodies are called autoantibodies. Depending on the type of lupus, a wide range of symptoms may be experienced, from rashes, hair loss, and achy, swollen joints to fever, anemia, and abnormal blood clotting. Though the disease can affect many parts of the body, individuals usually experience symptoms in only a few organs. There is no known cure for lupus. However,
Systemic Lupus Erythematosus, usually called as SLE or Lupus, is a type of incurable autoimmune disease which affects the hematologic, dermatologic, renal organ system and musculoskeletal. In other words, it attacks mostly the connective tissues of the body. Generally, an autoimmune disease happens when the immune system attacks healthy tissues of the body by producing protein called autoantibodies. This will cause inflammation and damage to the tissues. Inflammation causes indication of injuries such as redness, swelling and pain. The etiology of SLE is still unknown to the world. There is, however, increasing evidence that the presence and accumulation of apoptotic cells play a role in autoimmunity (White, S., and Rosen, A., 2003).
Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease that occurs when a person’s immune system attacks your own tissues and organs. SLE is characterized by the presence of autoantibodies directed against nuclear antigens. By definition, SLE is a multi-system disease, and patients can be infected in vastly different ways. SLE is the form of the disease that most people are referring to when they say “lupus.” The word “systemic” means the disease can affect not one, but many parts of the body (Johnson, 1999). SLE can affect every organ in the human body. The most common manifestations are rash, arthritis and fatigue. According to the Mayo Clinic, some complications of SLE are kidney failure, neurological problems, anemia,vasculitis,
SLE and any other autoimmune disorders usually tend to run in families. There is no clear pattern of inheritance or genes that causes SLE, People can inherit a gene variation through things like mutation which could lowen or increase the risk of SLE, but most commonly they dont inherit this disease itself. If mutations happen (which have very low chances) then SLE can be inherited froman autosomal recessive pattern. There are other reasons that may be genetically related but are still not found. Studies showed that the Major Histocompatibility Complex on chromosome 6 (which contains the human lymphocyte antigens) was the first genetically linked chromosome to SLE. The parts in a human lymphocyte antigen include important component in the immune
The pathogenesis of systemic lupus erythromatosus (SLE) is believed to be complex, owing to its autoimmune nature, variable clinical presentations and its multifactorial association with environmental and genetic factors [1]. Infections, as a major environmental factor have been implicated to play a role in the pathogenesis of SLE in genetically susceptible individuals [2]. Moreover, evidence suggests that SLE patients are more susceptible to a number of infections [3]. Epstein-barr virus (EBV) is one of the most studied infectious agent in these contexts. Some studies have shown that EBV is more prevalent among SLE patients especially those below 20 years of age compared to healthy individuals [4]. Higher levels of antibodies to early viral
Systemic Lupus Erythematosus is a chronic autoimmune disease which causes inflammation of your joints, tissues, and organs. The inflammation presents itself as heat, pain, swelling and redness. SLE is a variable disease that doesn’t take any one particular course; therefore its unpredictability makes it even more devastating. No two people will experience the same disease symptoms or severity level. As S.L.E progresses there will be periods of very subtle to no symptoms at all called remission or an exacerbation of symptoms called flares.
Introduction : B lymphocytes are the effectors of humoral immunity and provides defense against pathogens by producing antibody. B cells constitute approximately 15% of peripheral blood leukocytes and arise from progenitors and precursors in the bone marrow. B lymphocytes undergo random immunoglobulin variable gene rearrangements at the heavy and light chain loci. These chains pair with the Igα and Igβ polypeptides to form the mature B-cell receptor which is then transported onto the cell surface where it can bind antigen and signal inside the cell. Different populations of B cells result in pre immune pools where each cell in these quiescent populations expresses a B cell antigen receptor with a unique specificity. The BCRs come in contact with their specific antigen and generate several intracellular signals are which leads activation, differentiation, and formation of plasma cells and memory B cells. This process mediates the response to subsequent antigen challenges. B lymphocytes play an essential role by not only producing antibodies but also functioning as antigen-presenting cells and certain B cells can also negatively regulate the immune response by producing regulatory cytokines and directly interacting with pathogenic T cells via cell to cell contact. Newly generated immature B cells are selected to enter the peripheral mature B-cell pool only if they do not