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Immune system
Sepsis
Neonatal sepsis
Abscesses
Type I hypersensitivity
Food allergy
Anaphylaxis
Asthma
Type II hypersensitivity
Immune thrombocytopenic purpura
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Goodpasture syndrome
Rheumatic heart disease
Myasthenia gravis
Graves disease
Pemphigus vulgaris
Type III hypersensitivity
Serum sickness
Systemic lupus erythematosus
Poststreptococcal glomerulonephritis
Type IV hypersensitivity
Graft-versus-host disease
Contact dermatitis
Transplant rejection
Graft-versus-host disease
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
X-linked agammaglobulinemia
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Thymic aplasia
DiGeorge syndrome
Severe combined immunodeficiency
Adenosine deaminase deficiency
Ataxia-telangiectasia
Hyper IgM syndrome
Wiskott-Aldrich syndrome
Leukocyte adhesion deficiency
Chediak-Higashi syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Thymoma
Ruptured spleen
Blood transfusion reactions and transplant rejection: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Posttransplant lymphoproliferative disorders, or PTLDs, are uncontrolled growths of cells called lymphocytes that may occur in transplant recipients after receiving a solid organ, such as a kidney or a lung, or stem cells.
Transplant recipients require medications to suppress their immune systems which may contribute to the development of a PTLD.
Normally, immune cells can differentiate between healthy “self” and “other” cells by inspecting for the presence or absence of the normal “self” major histocompatibility complexes, also called human leukocyte antigens, present on the surface of every cell that contains a nucleus.
Healthy “self” cells are left alone.
“Others” include cells from other people or donors and “self” cells that are infected, damaged, or stressed.
Lymphocytes, are a class of rapidly dividing cells and, therefore, tends to develop mutations more often.
B-lymphocytes, or B-cells, work to develop antibodies toward invading microbes.
There’s also two types of T-lymphocytes, or T-cells.
Cytotoxic T-cells can directly destroy “other” cells and helper T-cells assist other immune cells.
Normally, if B-cells start to replicate out of control, it's the T-cells that keep them in check, and keep the immune response organized.
When people receive a transplanted organ or stem cells, they also must take immunosuppressive medications to prevent the immune system from rejecting, or attacking, the transplant.
In PTLDs, immunosuppression also prevents the destruction of abnormal lymphocytes that exhibit uncontrolled replication.
Resulting uncontrolled growth of lymphocytes can either be a benign hyperplasia, meaning there’s a large collection of noncancerous cells, or the cells can become malignant, resulting in a cancer called lymphoma.
While PTLD may result from the overproduction of T-cells, it is more typically associated with the overproduction of B-cells.
Post-transplant lymphoproliferative disorders (PTLDs) are a group of lymphoid neoplasms characterized by uncontrolled growths of lymphocytes. It occurs after someone has received a solid organ or stem cell transplant that requires immunosuppressive medications to prevent transplant rejection. PTLDs are caused by Epstein-Barr virus (EBV) infection and can originate in either type of lymphocyte: B-cells or T-cells. Diagnosis involves blood tests, a biopsy, and imaging, while treatment may include surgery, chemotherapy, and radiation.
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