Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis (EAA) is a rare immune system disorder that affects the lungs.[1] It is an inflammation of the airspaces (alveoli) and small airways (bronchioles) within the lung, caused by hypersensitivity to inhaled organic dusts and molds.[2] People affected by this type of lung inflammation (pneumonitis) are commonly exposed to the dust and mold by their occupation or hobbies.[2]
https://en.wikipedia.org/wiki/Hypersensitivity_pneumonitis
Transplant rejection occurs when transplanted tissue is rejected by the recipient's immune system, which destroys the transplanted tissue. Transplant rejection can be lessened by determining the molecular similitude between donor and recipient and by use of immunosuppressant drugs after transplant.[1]
https://en.wikipedia.org/wiki/Transplant_rejection
Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterised by an exaggerated response of the immune system (a hypersensitivity response) to the fungus Aspergillus (most commonly Aspergillus fumigatus). It occurs most often in people with asthma or cystic fibrosis. Aspergillus sporesare ubiquitous in soil and are commonly found in the sputum of healthy individuals. A. fumigatus is responsible for a spectrum of lung diseases known as aspergilloses.
ABPA causes airway inflammation, leading to bronchiectasis—a condition marked by abnormal dilation of the airways. Left untreated, the immune system and fungal spores can damage sensitive lung tissues and lead to scarring.
The exact criteria for the diagnosis of ABPA are not agreed upon. Chest X-rays and CT scans, raised blood levels of IgE and eosinophils, immunological tests for Aspergillus together with sputum staining and sputum cultures can be useful. Treatment consists of corticosteroids and antifungal medications.
https://en.wikipedia.org/wiki/Allergic_bronchopulmonary_aspergillosis
Transfusion-associated graft-versus-host disease (TA-GvHD) is a rare complication of blood transfusion, in which the immunologically competent donor T lymphocytes mount an immune response against the recipient's lymphoid tissue.[1] These donor lymphocytes engraft, recognize recipient cells as foreign and mount an immune response against recipient tissues.[2] Donor lymphocytes are usually identified as foreign and destroyed by the recipient's immune system. However, in situations where the recipient is severely immunocompromised, or when the donor and recipient HLA type is similar (as can occur in directed donations from first-degree relatives), the recipient's immune system is not able to destroy the donor lymphocytes. This can result in transfusion associated graft-versus-host disease.
https://en.wikipedia.org/wiki/Transfusion-associated_graft-versus-host_disease
Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis(PSGN).[4] It can be a risk factor for future albuminuria.[5] In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used.[6] Acute glomerulonephritis resulted in 19,000 deaths in 2013, down from 24,000 deaths in 1990 worldwide.[7]
https://en.wikipedia.org/wiki/Acute_proliferative_glomerulonephritis
Goodpasture syndrome (GPS), also known as anti-glomerular basement membrane disease, is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs, glomerulonephritis,[1] and kidney failure.[2]It is thought to attack the alpha-3 subunit of type IV collagen, which has therefore been referred to as Goodpasture's antigen.[3] Goodpasture syndrome may quickly result in permanent lung and kidney damage, often leading to death. It is treated with medications that suppress the immune system such as corticosteroids and cyclophosphamide, and with plasmapheresis, in which the antibodies are removed from the blood.
The disease was first described by an American pathologist Ernest Goodpasture of Vanderbilt University in 1919 and was later named in his honor.[4][5]
https://en.wikipedia.org/wiki/Goodpasture_syndrome
Bullous pemphigoid is an autoimmune pruritic skin disease preferentially in older people, aged over 60, that may involve the formation of blisters (bullae) in the space between the epidermaland dermal skin layers. The disorder is a type of pemphigoid. It is classified as a type II hypersensitivity reaction, with the formation of anti-hemidesmosome antibodies.
https://en.wikipedia.org/wiki/Bullous_pemphigoid
Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis foetalis,[1] is an alloimmune condition that develops in a fetus at or around birth, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta. Among these antibodies are some which attack antigens on the red blood cells in the fetal circulation, breaking down and destroying the cells. The fetus can develop reticulocytosis and anemia. The intensity of this fetal disease ranges from mild to very severe, and fetal death from heart failure (hydrops fetalis) can occur. When the disease is moderate or severe, many erythroblasts (immature red blood cells) are present in the fetal blood, earning these forms of the disease the name erythroblastosis fetalis (British English: erythroblastosis foetalis).
HDFN represents a breach of immune privilege for the fetus or some other form of impairment of the immune tolerance in pregnancy. Various types of HDFN are classified by which alloantigen provokes the response. The types include ABO, anti-RhD, anti-RhE, anti-Rhc, anti-Rhe, anti-RhC, multiantigen combinations, and anti-Kell. Although global prevalence studies of the differential contribution of those types are lacking, regional population studies have shown the anti-RhD type to be the most common cause of HDFN, followed by anti-RhE, anti-RhC, and anti-Rhc.[2]
https://en.wikipedia.org/wiki/Hemolytic_disease_of_the_newborn
No comments:
Post a Comment