The Best Known Autoimmune Disease, Lupus
The best known autoimmune disease, Lupus
Systemic lupus erythematosus (Systemic lupus erythematosus or les) is one of the best known autoimmune diseases that affects a rather large core of the population, mostly adult women adult women. It is influenced by a multitude of factors from environmental to hormonal, the genetic factors being the determinants in the disease.
He is characterized by the activation and multiplication of self-reactive B lymphocytes and by the production of autoantibodies (which attack the individual who produces it), causing the formation of immune complexes and causing damage at the level of the tissue or organ in which they are established does not specify. Among the autoantibodies that are expressed in the LES, in most cases we can find double -chain DNA antibodies (anti DNASD).
The mechanism of action is quite complex and requires the participation of a multitude of component of the affected body, such as cytokines, dendritic cells, etc. He does not present them in the same way in all the affected people. Pathologies change depending on the body that affects, as the symptoms and treatments will be specific to the different patients.
Systemic lupus erythematosus is an autoimmune, chronic and inflammatory disease characterized by damage to any organ, cells and tissues. Being autoimmune there is a loss of tolerance, that is, discriminating the strange agents of their own agents, therefore the lymphocytes recognize these own antigens and cause their elimination with the production of antibody.
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These antibodies form immune complexes with the antigens that are deposited in the membranes, favoring that local inflammation occurs and consequently originate that damage. In addition, it is characterized by periodic recurrences of inflammation and joint injury, tendons, other types of connective tissues and some organs.
There have been enough studies in finding out what factor is the trigger in the disease. The studies have been established around three factors. The first factor to consider is the hormonal factor. As previously mentioned, the disease affects women mostly, but mainly harms adult women (in fertile times). This is due to the concentration of a hormone in the body, called estrogens.
It has been seen that estrogen concentration increases the loss of tolerance by reducing apoptosis and facilitating the perpetuation of self-reactive B lymphocytes, through the increase in gene expression of the T CD40L lymphocytes. This CD40L is the CD40 ligand of B lymphocytes, therefore this interaction of receptors is essential in the increase and differentiation of B lymphocytes. It has also been proven that in women who have passed menopause, the predisposition to suffering from the disease is much smaller, because they have low estrogen concentration. However, there have been evidence that there are other factors that will be the most frequently triggers in the disease.
Another factor to take into account is the environmental field, both infectious factors such as viruses and non -infectious factors as chemical products. Among the infected factors we can find the acquired immunodeficiency virus and retrovirus, although it is considered that they may be an indirect consequence of the disease and not many studies have been carried out in this field.
One of the non -infectious factors most linked to them are ultraviolet rays, since they cause a trigger for the immune response, when the disease occurs, it can cause an outbreak or alter the DNA and intracellular proteins so that they are taken as if They were antigens. It has even been seen that lupus can be induced by drug.
Finally we have to take into account that there is a genetic factor, in fact this factor is one of the most important, since it has been seen that the combination of a series of genes contributes to the disease suffering.
These genes belong to the major histocompatibility complex (MHC), although there are others that do not belong to MHC and that are those that control the production of cytokines, the proliferation of lymphocytes, hyperactivity and positive regulation of target antigens in some tissues.
Deficiencies has also been observed in complement system genes, affecting the elimination of immunocomplexes and apoptosis process, which leads to the failure of organism’s tolerance.
There are even some patients of the SLE, who presents a deficiency in FC receptors that leads to a bad regulation in the activation of B lymphocytes or an attenuation of inflammatory responses is not produced.
In conclusion so that a person can suffer from the disease, in addition to being a carrier of a combination of genes, he must undergo a combination of environmental factors to develop the lupus phenotype.
In this section, the antibodies found in the disease, the antigens that trigger that immune response and the mechanism of action that are carried out to produce the damage will be studied to produce the damage to produce the damage.
Normally in it the antigens are formed due to the bad regulation in the elimination of cell remains (DNA, RNA, nuclear proteins, etc.), that is to say in apoptosis. In healthy people, the phagocytic system (macrophages among others) degrade these remains before their release, however in them they are transported in vesicles to be released without prior degradation or are established on the surface of the granules of the phagocytic cells. Therefore the phagocytic system cannot perform its function correctly, involving these apoptotic cells as a constant origin of antigens.
As mentioned above there are important genes in the MHC, specifically these are located on chromosome 6. These genes encode HLA antigens that act in the susceptibility and persistence of the disease. The HLA antigens that have been found in numerous studies in lupus are DR2 and DR3.
Other antigens that we can find are nuclear antigens, cell membrane antigens, plasma proteins and extracellular matrix. As we see, they are all components of the organism itself, being the most studied and that nuclear antigens are in greater proportion.
We can see that in the them there is an exclusive antigen of the disease that is located in greater proportion within the nuclear antigens, we refer to the double chain DNA (DNASD). Although we can also find other antigens such as simple chain DNA and rna antigens such as SM, ro, rnp, histones and chromatins. Each of these antigens will affect different tissues, cells or organs.
In conclusion, the constant existence of antigens in lupus is determined by genetic factors and the loss of tolerance that leads to the bad regulation of apoptosis.
The autoantibodies are a type of antibodies that are erroneously directed towards the organs or tissues of the organism itself. The immune system can produce one or several antibodies when it fails to identify between pathogenic and own proteins. These occur thanks to the proliferation of B lymphocytes, whose mechanism will be explained later.
We will focus on the main autoantibody of which is the specific anti-DNASD antibody, although there are other types of antibodies such as anti-rro, anti-la, etc.
Double chain anti-DNA antibodies (anti-DNASD) are part of a group of autoantibodies that are known as nuclear antibodies (ANA) and are immunoglobulins that react against different nuclear components of the organism. These antibodies incorrectly attack these organism components, producing a series of injuries.
In blood circulation we can find 3 main Ana types. The first one is known as natural ana and are found in all organisms under minimum values. The second type of Ana is activated as a result of infectious processes and when this process decreases, the values of this type of Ana also make them. Finally we can find the third type of Ana that are those that occur in autoimmune responses and are those that cause the loss of that tolerance and its origin is multifactoriral. This is the typical Ana that presents the lupus.
Set of procedures carried out
Lupus produces many mechanisms in the trigger of the disease, affecting many of the components presented by the immune system, such as B and T lymphocytes, cytokines, complement system, MHC, etc.
As we have commented on lupus, it is identified by the activation and hyperactivity of the B and T lymphocytes and the autoantibodies formation, which are regulated by the release of various cytokines produced by the T lymphocytes. These cytokines favor the proliferation of B lymphocytes and activate the secretion of IgG and IgM antibodies by joining it strongly to the antigen
The main indicators that the disease is taking.
The beginning of the disease occurs when there is an interruption in the tolerance of the B and T lymphocytes self-reactive, this means that the lymphocytes recognized. Apoptosis deficiency causes these self-reactive clones not to be eliminated and as a consequence they trigger the autoimmune response.
This causes a deficiency in the elimination of cell remains or apoptotic bodies by phagocytic cells, whose remains are admitted to vesicles for subsequent release or interact with receptors on the surface of apoptotic cells. In any case there is a constant reproduction of autoantigens. As responses to these autoantigens, the organism generates autoantibodies.
Once it is located in the bloodstream, both are joined and form antibody-antigen complexes that are called immune complex Appearance of the inflammatory process. Complement activation is because C1Q binds to apoptotic cells and does not allow these complexes to be phagocyted by macrophages efficiently.
Not all immune complexes are going to be deposited in the membrane, others will join the FC (FCyriiα) receptor found in dendritic cells, especially plasmocytoid dendritic cells or can be joined to the specific B -lymphocyte antigen receptor. Once the receiver has been coupled, they are internalized in endosome.
When these immune complexes have joined with the TLL receptors, they activate cinases that lead to the synthesis of the alpha interferon (INF-α) called type 1 interferon, whose main function is the induction of apoptosis or stimulation of the gene expression of apoptosis.
Once the activation of the type 1 interferon has occurred, the activation of the self-reactive T cells is stimulated. These self-reactive T lymphocytes will interact with B lymphocytes.
Regarding the constant activation of B lymphocytes, the existence of an activating B lymphocyte (Baff) factor can be observed, this factor can induce the response of the B lymphocytes independent of the T lymphocyte production and is regularized by the INFG factor , since it can influence the antibody class secreted by B lymphocytes and participate by increasing the expression of MHC of classes II, increasing its expression in the CPA and the consequent stimulation in the production of antibody. In addition, constant activation is also favored by interleukine 6 and interleukine 10. The first intervenes in the production of different kinds of immunoglobulins and in the differentiation of B lymphocytes and the second can regulate inflammatory responses and promotes the activation of B lymphocytes. In addition interleucin 4, 6 and 10 favors the response of TH2 that presents a clear participation with the INFG at the beginning of the disease.
These B lymphocytes and T lymphocytes interact at the binding site of the t lymphocyte receptors with the antigen, producing an coupling of the CD40 molecules of the B lymphocytes as an antigen presenter and its CD40L ligand of the T lymphocytes. This causes the production of cytokines, which act on the B lymphocyte with the consequent antibody production. Antigens that bind to immunoglobulins on the surface of B lymphocytes regulate the production of IgG antibodies, which causes cell growth. Its presence symbolizes that the activation of B lymphocytes is continuously and selectively.
All these processes lead to the production of immune complexes and the activation of cytotoxic T lymphocytes that provide autoanthogens, starting the entire cycle of the LES.
Symptomatology and possibility of treatment
As for symptoms and treatment we can find many manifestations due to the disparity of the disease. The most common effects are on the skin, such as photosyblity (reaction generated due to sun exposure), temporary alopecia in times of relapse and sores in the mouth. The useful symptoms for diagnoses and that are exclusive to the disease are erythema in butterfly wings and the appearance of varied red circles in shape and size. The Lupus not only affects tissues can also affect organs such as celebrating psychosis, depression …, to the heart, lungs (pleura) and kidneys referring to heart and respiratory insufficiencies and nephritis, among others. (Figure Presentation)
People who suffer from the disease have no cure but a series of treatments to reduce the effects on organs and tissues. However, there is no universal treatment because as the disease affects each person is very specific. With the treatment it is intended to reduce inflammation, inhibit the hyperactivity of T and B lymphocytes, avoid recurrences, monitor clinical manifestations and reduce lesions caused, ultimately improve patients’ lives. The most used medications in treatments are anti -inflammatories, corticosteroids, antipalúdico and immunosuppressive medications (immunological modulators).
As a curiosity the name comes because doctors observed a cutaneous eruption on patient’s face. This eruption looked like a wolf’s face, whose name in Latin is lupus.
We can conclude by saying that many studies are still needed in terms of the participation of each of the components of the immune system in the disease and of all those external factors that interact in their phenotype, in order to act effectively on those roads that have a bad regulation or deficiency in their mechanisms of action, to more definitively alleviate all symptoms and improve the quality of life of all patients suffering from the disease.
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