Immunoglobulin A

INTRODUCTION:
  • 0-13% of Ig
  • Normal serum level: 0.6-4.2 mg/ml
  • Half-life: 6-8 days
  • 5-8% of serum Ig
  • Commonest immunoglobulin deficiency is of IgA
STRUCTURE:
  • 2 forms: Serum IgA - monomer (75 molecule)
  • Secretory IgA (SIgA) is dimeric formed by two monomers joined by J chain, synthesized by plasma cells.
  • In Serum 90% occurs as monomer and 10% as dimer.
  • In Secretions (sIgA) 90% occurs as Dimer and 10% as monomer.
PROPERTIES:
  • It is 2nd highest serum Ig
  • Major secretory Ig (Mucosal or Local Immunity)
  • The secretory component of SigA is produced by mucosal and glandular epithelial cells
  • SIgA is selectively concentrated in secretions on mucus surfaces forming an antibody paste
  • SIgA plays an important role in local immunity against respiratory and intestinal pathogens
  • Tears, saliva, gastric and pulmonary secretions and serves as first lie of defense against microorganism invasion.
  • IgA does not fix complement but activates alternative complement pathway
  • Can't cross placenta
  • Predominant type of immunoglobulin in human milk 
  • Temp 37c
SUBTYPES:
  • IgA1 - Alpha 1 (α1) heavy chains
  • IgA2 - Alpha 2 (α2) heavy chains
LOCATION:
  • IgA is found in peyer's patch 
  • The direct secretion of secretory IgA onto mucosal epithelia represents the major effector mechanism of mucosa-associated lymphoid tissue (MALT).
  • IgA is the main immunoglobulin in secretions such as milk, saliva, and tears and in secretions of the respiratory, intestinal, and genital tracts. 
  • It protects mucous membranes from attack by bacteria and viruses.
IMMUNITY:
  • IgA nephropathy may occur following an episode of mucus membrane infection of the respiratory or gastrointestinal tract.
  • Genetically susceptible individuals show increased amounts of IgA production following a viral or bacterial infection of the mucous membrane.
  • Circulating IgA containing immune complexes are formed which later are deposited in the mesangium of the glomeruli of the kidney resulting in glomerulopathy.
  • Henoch-Schonlein purpura is characterized by the deposition of IgA around the vessels 
IgA DEFICIENCY:
  • IgA deficiency is often familial
  • In Protein Energy Malnutrition IgA is reduced the most
  • In malnourished subjects(e.g.kwashiorkar), secretory IgA is generally reduced. Therefore infections tend to be severe and recovery delayed
  • It may be acquired by :
  • Congenital infections such as toxoplasmosis, rubella, CMV
  • Treatment with phenytoin
  • v Pathogenesis -
  • Block in B cell differentiation due to defective interaction between T and B cells. Naive B cells are not able to differentiate into IgA - producing cells.
Features
  • Respiratory infections
  • Chronic diarrheal diseases
  • Increased incidence of asthma and other atopic disease
  • Frequent production of autoantibodies
  • Association with arthritis and SLE
  • Reduction of IgG2 and IgG4
Treatment -
  • Symptomatic
  • No benefit of immunoglobulin (IgA) infusion because of increased risk of development of autoantibodies against IgA.
  • Exceptionally immunoglobulin infusion may help in patients with IgG2 and IgG4 deficiency.
Exam Question
  • Immunoglobulin in peyer's patch is IgA
  • IgA is the main immunoglobulin in secretions
  • Commonest immunoglobulin deficiency is of IgA
  • IgA nephropathy may occur following an episode of mucus membrane infection of the respiratory or gastrointestinal tract.
  • IgA is formed by two monomers joined by J chain
  • IgA is associated with immunity of intestine and respiratory epithelium
  • IgA is rich in serum and body secretions
  • IgA activates complement by alternate pathway
  • Predominant type of immunoglobulin in human milk is IgA
  • In Protein Energy Malnutrition IgA is reduced the most
  • Henoch-Schonlein purpura is characterized by the deposition of IgA around the vessels 
  • In Kwashiorkor,IgA is most affected
  • Acquire IgA deficiency may occur in Severe Congenital toxoplasmosis
  • IgA is present in local mouth secretions

Don't Forget to Solve all the previous Year Question asked on Immunoglobulin A