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Immunoglobulin M (IgM) is the largest of several isotypes of antibodies (also known as immunoglobulin) that are produced by vertebrates. IgM is the first antibody to appear in the response to initial exposure to an antigen ; [ 1 ] [ 2 ] causing it to also be called an acute phase antibody.
Immunodeficiency with hyper IgM type 2 is caused by a mutation in the Activation-Induced Cytidine Deaminase gene, which is located on the short arm of chromosome 12.. The protein that is encoded by this gene is called Activation-Induced Cytidine Deaminase (AICDA) and functions as a DNA-editing deaminase that induces somatic hypermutation, class switch recombination, and immunoglobulin gene ...
Immunodeficiency with hyperimmunoglobulin M is a rare disorder characterized by recurrent infections, low or absent IgG, IgE, and IgA levels, and normal or elevated levels of IgM and IgD. [ 2 ] : 84
Hyper IgM syndrome is a rare primary immune deficiency disorders characterized by low or absent levels of serum IgG, IgA, IgE and normal or increased levels of serum IgM. [ 8 ] They are resulting from mutations in the pathway from B-cell activation to isotype class switching.
Rheumatoid factor (RF) is the autoantibody that was first found in rheumatoid arthritis.It is defined as an antibody against the Fc portion of IgG and different RFs can recognize different parts of the IgG-Fc. [1]
μ – IgM; There are also two light chain isotypes κ and λ; however, there is no significant difference in function between the two. Thus an antibody isotype is determined by the constant regions of the heavy chains only. [1] IgM is first expressed as a monomer on the surface of immature B cells.
Hyper IgM syndromes is a group of primary immune deficiency disorders characterized by defective CD40 signaling; via B cells affecting class switch recombination (CSR) and somatic hypermutation. Immunoglobulin (Ig) class switch recombination deficiencies are characterized by elevated serum IgM levels and a considerable deficiency in ...
Secondary cold agglutinin syndrome occurs when autoantibodies bind to red blood cells, rendering them subject to attack by the complement system. [17] It is a result of an underlying condition potentially associated with either monoclonal cold-reacting autoantibodies or polyclonal cold-reacting autoantibodies [16] predominantly caused by infection or lymphoproliferative disorders. [16]