5. Please analyze the relationship between pathogenic infection and autoimmune diseases.
Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors,age , environmental triggers such as particular viruses, bacteria and other infectious pathogens play a major role in the development of autoimmune diseases.
Multiple arms of the immune system may be involved in autoimmune pathology. antigen-presenting cells (APCs) , major histocompatibility complex (MHC) ,Cytolytic T cells ,T helper cells release cytokines that can lead to direct effects or can activate macrophages, monocytes and B cells, Fc receptor.
There are multiple mechanisms by which host infection by a pathogen can lead to autoimmunity
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This kind of immune response to a persisting pathogen, or direct lysis by the persisting pathogen, causes damage to self-tissue and releases antigen from damaged tissue are taken up by APCs, and this initiates a self-specific immune response. ‘A domino effect can occur, where the non-specific activation of one arm of the immune system leads to the activation of other arms. infection may lead autoimmunity through the processing and presentation of ‘cryptic antigens’. In contrast to dominant antigenic determinants, subdominant cryptic antigens are normally invisible to the immune system. The inflammatory environment that arises after infection can induce increased protease production and differential processing of released self-epitopes by APCs.Bystander activation’ describes an indirect or non-specific activation of autoimmune cells caused by the inflammatory environment present during …show more content…
Because viral genome can be detected after infectious virus has been cleared from the heart, latent virus may attract inflammation during the chronic stage of disease. However, when we examined the heart for the presence of latent MCMV, we found that viral genome and transcript were present in mice both susceptible to and resistant to the development of chronic disease. These results indicate that persistence of virus alone is not the determining factor in the development of chronic myocarditis. Yet the best evidence that active viral infection is not required for myocarditis to develop comes from the demonstration that injecting susceptible mice with cardiac myosin emulsified in adjuvant induces experimental autoimmune myocarditis. In fact, the pathogenesis of experimental autoimmune myocarditis closely resembles the biphasic myocarditis associated with CB3 or MCMV infection. This finding indicates that the adjuvant effect produced by infections or adjuvants
Acquired Immune System – Specific for distinct pathogens and the ability to create immunological memory; requires presentation of foreign antigens by antigen presenting cells(Rodriguez, 2014, p. 86).
A disorder where the body is attacking itself is known as an autoimmune disorder. In an autoimmune disorder the body cannot decipher between a pathogen, bacteria, or infection attacking the body and normal healthy body tissue. The majority of autoimmune disorders are long lasting or even permanent. An example of a chronic autoimmune disorder is multiple sclerosis (MS).
this occurs in a series of steps, the first of which is incorporation of unidentified antigens by APCs in the epidermis and dermis. This process involves binding of the antigens to the MHC on the APC surface and the APC migrates to the lymph nodes. There, the APC binds reversibly and briefly with naïve or resting T cells through interactions between surface molecules located on both cells. Next, the MHC presents the antigen to a T lymphocyte receptor to begin activation of the T lymphocyte. The second signal for T lymphocyte activation is a non-antigen/ cell-cell interaction known as costimulation. If costimulation does not occur, the T lymphocyte will either undergo apoptosis or become unresponsive. Costimulation involves pairing of receptor with ligand on the T cell; these pairs include (LFA)-3 interacting with CD2, B7 interacting with CD28, and ICAM-1 interacting with LFA-1 (Lebwohl, 2003).
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.
Overwhelming, deleterious host immune response to an infection due to release of chemicals to fight the infection 2• 1
There are more than a hundred autoimmune diseases. There are approximately 50 million people living with some form of an autoimmune disease in America. Depending on the type, an autoimmune disease can cause many different parts of your body to go under siege. Some of the most common autoimmune diseases are Systemic Lupus Erythematosus, Multiple Sclerosis, and Rheumatoid arthritis. The current medical system does not recognize Autoimmune illnesses as diseases of the immune system. Instead, they are classified as diseases of the specific organ that is affected. For example, someone with Celiac disease would see a gastroenterologist instead of someone who specializes in immune disorders. Even if a disease falls under the broad umbrella of immune disorder, there is not a unified medical treatment in order. each specialist has their own method of approach. My friend Mia Washington was diagnosed with Graves' disease at the tender age of 14. It was a frightening moment for her single working mother. As Mia's friend, it was a shock to me too. The odds weren't in our favor. Mia was always a sickly child, but soon after her diagnosis, she began to
Immunotherapy is a form of medical treatment intended to stimulate or restore the ability of the immune system to fight infection and disease. This can be by inducing, enhancing, or suppressing an immune response. Immunotherapies designed to elicit or amplify an immune response are classified as activation immunotherapies, while those that reduce or suppress immune response are suppression immunotherapies. Active immunotherapy has been effective against agents that normally cause acute self-limiting infectious disease. However, a more effective immunotherapy for chronic infectious diseases or cancer requires the use of appropriate target antigens; the
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
Autoimmune disease- any of a large group of diseases characterized by abnormal functioning of the immune system that causes your immune system to produce antibodies against your own tissues (the definition from wordnetweb.pronceton.edu).
When the pathogen replicates different components of immune system evolves to protect against various types of pathogens. However infection of an organism does not necessarily shows diseases, disease are only present when the bolus of infection, in terms of when immunity is comprised. All components of
Cytokines are cell signaling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection, and trauma. Researchers at UC Davis have found that early exposure to inflammatory cytokines can “paralyze” CD4 cells. This CD4 paralysis could play a role in preventing autoimmunity. Autoimmunity is misdirected immune responses that can cause the immune system to go awry and attack the body itself. By shutting down CD4 cells, it prevented an autoimmune response. This research shows the potential to paralyze the immune system to prevent autoimmunity, or to adjust and teach it to accept transplanted cells and
Do you feel fatigued even after you get a full night of sleep? Do you have achy muscles and joints, brain fog, inability to concentrate, or insomnia? Do you get rashes, eczema, hives, or skin irritation? Do you have an inability to tolerate cold or heat? Do you get diarrhea, bloating, constipation, or stomach pain? If you answered “yes” to several of these, there’s a good chance you have an autoimmune condition. Many people suffer for years with a vague set of symptoms that look like many other conditions but can’t be clearly defined or put in a box. Today we know this previous gray area actually defines the symptoms that precede or are involved in the process of autoimmunity.
With autoimmune diseases, the underlying issue is similar. The body's immune system becomes unable to recognize healthy cells from diseased cells. Consequently, the immune’s own defense mechanism produces antibodies that attack the normal tissues and cells. Autoimmune diseases
Scientists who research the epidemiology of autoimmune diseases have experienced many complications in their work. In a field where one plus one rarely equals two, researchers have been work fervently to determine which cell types are responsible for, or at least involved in, autoimmune dysfunction. The main subject of study by Esposito et al. is the deleterious effects of chronic activation of proinflammatory cytokines. To this end, this team has sought to characterize and quantify the cells found in various loci in mice plagued with relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), an induce murine model of human multiple sclerosis (MS). Another question of paramount importance is how to elucidate the mechanisms of these cells and their specific cell markers. For example, are certain cells present only in the target organ? Or did these cells migrate to that location? Or were there sequential stages of differentiation that occurred? Or is it a combination of the aforementioned postulates?
There are two branches of the immune response: the innate immune response and the adaptive immune response. The innate immune response consists of multiple leukocytes that recognize pathogen associated molecular patterns (PAMPs) [1]. These PAMPs are non-specific, conserved motifs present on a broad range of pathogens, and are recognized through various pattern recognition receptors (PRRs) on leukocytes, which trigger a pro-inflammatory response [1]. Conversely, the adaptive immune response is composed of only two leukocytes, B lymphocytes and T lymphocytes. Both subsets of lymphocytes have the capacity to generate an immune response specific to the invading pathogen [1]. In order for this to occur, the adaptive immune system must be able to recognize specific foreign antigens, as opposed to conserved motifs. Thus, stringent regulation of both B and T lymphocytes must occur in order to prevent recognition of self-antigens as foreign; this process is termed self-tolerance. Self-tolerance occurs through two mechanisms. The first is central tolerance, which takes place in the thymus (T cells) and bone marrow (B cells) [2]. Central tolerance selects for individual B and T cells, which do not recognize self-antigens presented to them in the primary lymphoid organs, to continue maturation [2]. The second is peripheral tolerance, which occurs outside of primary lymphoid organs, where B and T lymphocytes are further selected for self-reactivity to antigens that were not presented to