Immune disorders can be generally classified as immune over-reaction (such as allergy, asthma, and allergic rhinitis which is also called hay fever), under-reaction (such as AIDS, please see details under "Infectious Diseases"), and auto-reaction (such as rheumatoid arthritis, lupus, multiple sclerosis, and diabetes). Organ transplantation is a cause of immune disfunction because of immune rejection. How can QIAGEN's immunology-related PCR arrays and Epigenetic PCR arrays help you with your research?
See details here.
An allergic response is the result of an immune over-reaction
(hyper-sensitivity), leading to the activation of Th2 (T helper 2 cell)
responses, such as production of IL-4, IL-5, and IL-13 from CD4+ T cells. Th2
cell-driven inflammation is an abnormal response to harmless airborne particles.
IgG1 or IgE from B-cells is also responsible for allergic reaction. Dendritic
cells, epithelial cells, and basophils are the major players in the initiation
of Th2 response. Please use QIAGEN's Th1/Th2/Th3 PCR arrays, T-Cell and
B-Cell Activation PCR arrays, and Dendritic and Antigen Presenting Cell PCR
arrays to discover genes responsible for the allergic response including
asthma.
Asthma is also characterized by Th2 type inflammation, leading to airway
hyper-response and tissue remodeling. Activated mast cells, eosinophils, and
basophils infiltrate the airways as a result of an excessive Th2 cell immune
response. These innate effectors and airway epithelial cells can also augment
and bypass the traditional Th2 cell-mediated allergic inflammation.
Asthma and chronic obstructive pulmonary disease (COPD) are the two most
common chronic respiratory diseases. COPD, predominantly as a result of tobacco
smoke exposure, is the fourth leading cause of mortality worldwide. COPD is
characterized by an irreversible limitation on pulmonary airflow associated with
chronic inflammation and mucous hypersecretion (chronic bronchitis) and/or the
pathological destruction of alveolar airspaces. COPD patients exhibit many of
the characteristics of a classical autoimmune response.
Autoimmune diseases are characterized by self-reactive immune processes
mediated by T- and B-cells. Autoimmunity is believed to develop when genetically
predisposed individuals encounter environmental agents that trigger the
response. Interactions between genetic elements and epigenetic changes caused by
environmental agents are responsible for inducing autoimmune disease. These
disorders exhibit a spectrum of clinical features that range from local or
organ-specific (thyroid, liver, kidney, artery, joint...) to systemic diseases.
Both innate and adaptive immunity are responsible for autoimmunity. It has been
recognized recently that similarities of autoimmune diseases significantly
outnumber differences in terms of pathogenesis and mechanisms. Loss of self
tolerance is fundamental to autoimmunity. The failure of regulatory T cells to
maintain immune tolerance and inefficient clearance of dead cells are two common
mechanisms of autoimmune disorders. QIAGEN's Inflammatory Response and
Autoimmunity PCR arrays, Inflammatory Cytokines and Receptors PCR arrays, Th17
for Autoimmunity and Inflammation PCR arrays, Innate and Adaptive Immune
Response PCR arrays, Interferon alpha, beta Response PCR arrays, T-Cell Anergy and
Immune Tolerance PCR arrays, Inflammatory Receptors Epigenetic ChIP PCR arrays,
Inflammatory Response Methylation PCR arrays, T-Cell Activation Methylation PCR
arrays, and Cytokine Production Methylation PCR arrays are all powerful tools
for studying autoimmunity.
Rheumatoid arthritis is a chronic systemic inflammatory disease primarily
affecting the synovium (a thin layer of tissue only a few cells thick which
lines the joints and tendon sheaths) of diarthrodial joints (freely moveable
joints held together by a joint capsule, such as the knee and shoulder).
Rheumatoid factor is an auto-antibody (an antibody directed against self
tissues) against the Fc portion of IgG, which is itself an antibody. Rheumatoid
factor and IgG join to form immune complexes. Patients with rheumatoid arthritis
are at increased risk of mortality largely attributed to increased
cardiovascular death. Interplay between IL-17A and other Th17 cytokines such as
IL-17F, IL-22, and IL-21 is evident in the pathoimmunological process. TNF-positive
Th17 cells potentially cause persistent arthritis in human. TNF inhibitors have
shown promising results to treat rheumatoid arthritis.
Rheumatoid arthritis is sometimes confused with osteoarthritis.
Osteoarthritis is a group of degenerative diseases involving degradation of
joints. A common misconception is that osteoarthritis is due to wear and tear.
Loss of cartilage is the major cause of osteoarthritis, as the body struggles to
mend ongoing damage, immune and regeneration processes can accelerate damage.
Systemic lupus erythematosus (SLE) (lupus) is an autoimmune disease that
primarily affects females with the involvement of multiple organs including the
kidneys, joints, nervous, and blood system. The production of antibodies against
cell nuclear structures causes the initiation of chronic autoimmunity in lupus.
Again, lupus is characterized by quantitative and/or qualitative deficiencies of
regulatory T cells. Patients with lupus have an increased risk of premature
thrombosis. Antiphospholipid antibodies probably play a key role in the
development of thrombosis by affecting cell surfaces as well as platelet
function.
Data from retrospective and prospective epidemiological studies strongly
suggest that the infection by enteroviruses, such as coxsackievirus B, is
important in the development of type 1 diabetes mellitus. Through the infection
of pancreatic beta cells and the activation of innate immunity and inflammation,
virus-induced interferon alpha can act as an initiator of autoimmunity directed
against beta cells. Multiple sclerosis (MS) is a chronic immune-mediated
demyelinating disease of the central nervous system that often affects young
females. Type 1 diabetes and multiple sclerosis have been largely viewed as
different, organ-specific diseases with different managements, however,
strikingly similar features are observed between these two diseases. Both
diseases result from a combination of genetic factors and environmental risk
factors. For example, the human leukocyte antigen (HLA) complex and IL2RA are
the common susceptibility genes for both diseases and enterovirus infection is
associated with diabetes, Epstein-Barr virus with multiple sclerosis.
The initial sensing of infection is mediated by innate pattern recognition
receptors (PRRs), which include Toll-like receptors (TLRs), RIG-I-like
receptors, NOD-like receptors, and C-type lectin receptors. The intracellular
signaling cascades triggered by these PRRs lead to transcriptional expression of
inflammatory mediators that coordinate the elimination of pathogens and infected
cells. However, aberrant activation of this system leads to immunodeficiency,
septic shock, or induction of autoimmunity. It is thought that, similar to
recognition by TLRs, pathogen-associated molecular patterns interact with the
leucinerich-repeat domains of NALPs, leading to activation of the inflammasome.
The inflammasome is a cytosolic, multiprotein platform that allows activation of
precursors of proinflammatory caspases, which then cleave the precursor of
interleukin-1beta (pro-IL-1beta) into the active form, the secretion of which leads to
a potent inflammatory response. The central components of an inflammasome are
members of the NALP family. NALP1, NALP2 and NALP3 have been shown to form
inflammasomes, and the importance of NALP3 is well established since mutations
in the gene that encodes NALP3 (CIAS1) cause autoinflammatory disorders. TLRs
and NALP3 induce immune responses through recognition of the same or similar
microbial structures and that IL-1beta secretion is independently regulated by two
mechanisms: the first is TLR-dependent and results in NFkB-mediated
transcription of the gene that encodes pro-IL-1beta, and the second is
NALP3-dependent and results in cleavage of pro-IL-1beta into IL-1beta. QIAGEN's
Toll-Like Receptors PCR arrays and Inflammasomes PCR Arrays can be used to study
the involvement of TLRs and inflammasomes in immune disorders.
Another form of immune response is immune rejection caused by organ
transplantation, which is often used to rescue the terminal stages of renal,
cardiac, hepatic, and pulmonary diseases. Graft rejection, immunosuppression,
and anti-infection, however, still remain as the major challenges in clinical
practice. Rejection caused by mismatched human leukocyte antigen (HLA) is an
adaptive immune response and is mediated through both T-cell and humoral immune
(antibodies) mechanisms. Taken together, QIAGEN provides a broad range of
discovery tools for studies of immune disorders.
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