Autoimmune Hemolytic Anemia

Mark A. Vickers, Robert N. Barker

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Autoimmune hemolytic anemia (AIHA) is a classic example of type II hypersensitivity, caused by autoantibodies that bind red blood cells (RBC). The autoantibodies can be divided into cold or warm types, depending on the optimum temperature at which they bind, and AIHA can also be classified as either primary or secondary if there is an underlying disease such as neoplasia or infection. Hemolysis results from complement fixation leading to membrane attack complex formation, or phagocytosis mediated by receptors for IgGFc and C3. The pathogenicity of cold autoantibodies depends on their thermal amplitude, and on titer, isotype, and phagocyte activation state for warm antibodies. Multiple genetic and environmental factors contribute to susceptibility. Cold autoantibodies most commonly recognize the I blood group, and warm autoantibodies the Rh complex. Studies of responses to RBC autoantigens indicate that warm antibody production is helper dependent and associated with failure of peripheral self-tolerance mechanisms.

Original languageEnglish
Title of host publicationThe Autoimmune Diseases
EditorsIan Mackay, Noel R Rose
PublisherElsevier Inc
Pages649-661
Number of pages13
Edition5
ISBN (Print)9780123849298
DOIs
Publication statusPublished - Dec 2013

Fingerprint

Autoimmune Hemolytic Anemia
Autoantibodies
Erythrocytes
Peripheral Tolerance
Complement Membrane Attack Complex
Self Tolerance
Autoantigens
Phagocytes
Blood Group Antigens
Hemolysis
Antibody Formation
Virulence
Hypersensitivity
Hot Temperature
Temperature
Antibodies
Infection
Neoplasms

Keywords

  • Anemia
  • Autoantibody
  • B cell
  • Complement
  • Hemolysis
  • Immunological tolerance
  • Macrophage
  • Phagocytosis
  • Red blood cell
  • T helper cell
  • Type II hypersensitivity

ASJC Scopus subject areas

  • Immunology and Microbiology(all)

Cite this

Vickers, M. A., & Barker, R. N. (2013). Autoimmune Hemolytic Anemia. In I. Mackay, & N. R. Rose (Eds.), The Autoimmune Diseases (5 ed., pp. 649-661). Elsevier Inc. https://doi.org/10.1016/B978-0-12-384929-8.00046-0

Autoimmune Hemolytic Anemia. / Vickers, Mark A.; Barker, Robert N.

The Autoimmune Diseases. ed. / Ian Mackay; Noel R Rose. 5. ed. Elsevier Inc, 2013. p. 649-661.

Research output: Chapter in Book/Report/Conference proceedingChapter

Vickers, MA & Barker, RN 2013, Autoimmune Hemolytic Anemia. in I Mackay & NR Rose (eds), The Autoimmune Diseases. 5 edn, Elsevier Inc, pp. 649-661. https://doi.org/10.1016/B978-0-12-384929-8.00046-0
Vickers MA, Barker RN. Autoimmune Hemolytic Anemia. In Mackay I, Rose NR, editors, The Autoimmune Diseases. 5 ed. Elsevier Inc. 2013. p. 649-661 https://doi.org/10.1016/B978-0-12-384929-8.00046-0
Vickers, Mark A. ; Barker, Robert N. / Autoimmune Hemolytic Anemia. The Autoimmune Diseases. editor / Ian Mackay ; Noel R Rose. 5. ed. Elsevier Inc, 2013. pp. 649-661
@inbook{a9cbfcd8786d402bbd8840378f24ce7a,
title = "Autoimmune Hemolytic Anemia",
abstract = "Autoimmune hemolytic anemia (AIHA) is a classic example of type II hypersensitivity, caused by autoantibodies that bind red blood cells (RBC). The autoantibodies can be divided into cold or warm types, depending on the optimum temperature at which they bind, and AIHA can also be classified as either primary or secondary if there is an underlying disease such as neoplasia or infection. Hemolysis results from complement fixation leading to membrane attack complex formation, or phagocytosis mediated by receptors for IgGFc and C3. The pathogenicity of cold autoantibodies depends on their thermal amplitude, and on titer, isotype, and phagocyte activation state for warm antibodies. Multiple genetic and environmental factors contribute to susceptibility. Cold autoantibodies most commonly recognize the I blood group, and warm autoantibodies the Rh complex. Studies of responses to RBC autoantigens indicate that warm antibody production is helper dependent and associated with failure of peripheral self-tolerance mechanisms.",
keywords = "Anemia, Autoantibody, B cell, Complement, Hemolysis, Immunological tolerance, Macrophage, Phagocytosis, Red blood cell, T helper cell, Type II hypersensitivity",
author = "Vickers, {Mark A.} and Barker, {Robert N.}",
year = "2013",
month = "12",
doi = "10.1016/B978-0-12-384929-8.00046-0",
language = "English",
isbn = "9780123849298",
pages = "649--661",
editor = "Ian Mackay and Rose, {Noel R}",
booktitle = "The Autoimmune Diseases",
publisher = "Elsevier Inc",
edition = "5",

}

TY - CHAP

T1 - Autoimmune Hemolytic Anemia

AU - Vickers, Mark A.

AU - Barker, Robert N.

PY - 2013/12

Y1 - 2013/12

N2 - Autoimmune hemolytic anemia (AIHA) is a classic example of type II hypersensitivity, caused by autoantibodies that bind red blood cells (RBC). The autoantibodies can be divided into cold or warm types, depending on the optimum temperature at which they bind, and AIHA can also be classified as either primary or secondary if there is an underlying disease such as neoplasia or infection. Hemolysis results from complement fixation leading to membrane attack complex formation, or phagocytosis mediated by receptors for IgGFc and C3. The pathogenicity of cold autoantibodies depends on their thermal amplitude, and on titer, isotype, and phagocyte activation state for warm antibodies. Multiple genetic and environmental factors contribute to susceptibility. Cold autoantibodies most commonly recognize the I blood group, and warm autoantibodies the Rh complex. Studies of responses to RBC autoantigens indicate that warm antibody production is helper dependent and associated with failure of peripheral self-tolerance mechanisms.

AB - Autoimmune hemolytic anemia (AIHA) is a classic example of type II hypersensitivity, caused by autoantibodies that bind red blood cells (RBC). The autoantibodies can be divided into cold or warm types, depending on the optimum temperature at which they bind, and AIHA can also be classified as either primary or secondary if there is an underlying disease such as neoplasia or infection. Hemolysis results from complement fixation leading to membrane attack complex formation, or phagocytosis mediated by receptors for IgGFc and C3. The pathogenicity of cold autoantibodies depends on their thermal amplitude, and on titer, isotype, and phagocyte activation state for warm antibodies. Multiple genetic and environmental factors contribute to susceptibility. Cold autoantibodies most commonly recognize the I blood group, and warm autoantibodies the Rh complex. Studies of responses to RBC autoantigens indicate that warm antibody production is helper dependent and associated with failure of peripheral self-tolerance mechanisms.

KW - Anemia

KW - Autoantibody

KW - B cell

KW - Complement

KW - Hemolysis

KW - Immunological tolerance

KW - Macrophage

KW - Phagocytosis

KW - Red blood cell

KW - T helper cell

KW - Type II hypersensitivity

UR - http://www.scopus.com/inward/record.url?scp=84902614658&partnerID=8YFLogxK

U2 - 10.1016/B978-0-12-384929-8.00046-0

DO - 10.1016/B978-0-12-384929-8.00046-0

M3 - Chapter

SN - 9780123849298

SP - 649

EP - 661

BT - The Autoimmune Diseases

A2 - Mackay, Ian

A2 - Rose, Noel R

PB - Elsevier Inc

ER -