Serum sickness is a Type 3 hypersensitivity reaction, in which the body responds to antigenic medical substances and produces antibodies. These antibodies in circulation then bind to the antigenic drugs and set off the complement cascade. Rheumatoid arthritis is also a Type 3 hypersensitivity reaction.
A) Apoptosis of macrophages- apoptosis is generally not a type of hypersensitivity reaction. B) Mast cel degranulation- this is part of a Type 1 hypersensitivity reaction/anaphylaxis, in which mast cells bind IgE on their surface, and IgE binding to the target antigen induces a conformational change in the IgE that sets off mast cell degranulation. C) Natural Killer Cell killing- plays a variety of roles, including cancer suppression and destruction of virally infected cells. If they play a role in hypersensitivity, it is part of Type 2 HSR in which they would respond to Ig on the cell surface. E) Wheel and flare reactions- This is also a Type 1 HSR.
bumping the OP; extraarticular manifestations are common in RA (i.e. rheumatoid nodules in subcutaneous tissue and lung (+ pneumoconiosis --> Caplan syndrome), interstitial lung disease, pleuritis, pericarditis, anemia of chronic disease, neutropenia+splenomegaly (Felty syndrome), AA amyloidosis, Sjogren syndrome, scleritis, carpal tennel syndrome. (btw I thought RA was local and HSR II)
Maybe they went with serum sickness (a type III hypersensitivity rxn) on this question based on the serology used to diagnose RA. Pts with RA have antibodies to immunoglobulin G (IgG), called rheumatoid factors (RFs). It makes some sense that upon these rheumatoid factors reacting with "self" circulating IgG, immune complexes would form that would later deposit in tissues (explaining in part the extraarticular manifestations seen with RA, ex. rheumatoid nodules, pleuritis, pericarditis etc..)
https://www.sciencedirect.com/topics/medicine-and-dentistry/type-iii-hypersensitivity
Serum sickness—the prototypic immune complex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibody- antigen complexes form and deposit in tissues = complement activation = inflammation and tissue damage. Fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 1–2 weeks after antigen exposure. Serum sickness-like reactions are associated with some drugs (may act as haptens, eg, penicillin) and infections (eg, hepatitis B).
RA is a type 3 hypersensitivity reaction which has two components.
CD 4+ T cells will infiltrate tissue and react to autoantigens present in the synovial joint, this causes TNF-alpha and IL-1 to be released. These inflammatory cytokines will cause the initial inflammatory reaction. These cytokines ALSO activate B cells.
B cells produce rheumatoid factor as well as anti cyclic citrullinated peptide antibody. They bind the autoantigens and form IMMUNE complexes that deposit on the synovium. They cause complement to be activated. Hence the classic Type 3 hypersensitivity reaction, it is composed of 3 things: 1. antigen 2. antibody 3. complement
Next, you need to know that serum sickness (FA) is ALSO a type 3 hypersensitivity reaction, this time it is due to penicillin or a monoclonal antibody, basically some antigenic drug, which causes antibody to bind and then deposit complement.
Type III hypersensitivity is defined by the presence of circulating antigen-antibody-complement complexes that deposit in tissues and cause inflammation and destruction. (she had decreased C3)
type III hypersensitivity reactions: SLE, serum sickness reaction, polyarteritis nodosa(PAN), and post-streptococcal-glomerulonephritis(PSGN). RA is also a mixed Type 3 and Type 4 HSR.
Serum sickness occurs when a drug, such as anti-thymocyte globulin, acts as a hapten to the immune system, triggering antibody formation. Serum sickness reaction usually occurs 1 to 2 weeks after the initial exposure to the drug, reflecting the time required to mount an immune response. The antibodies then bind the drug, deposit in tissue, and attract and activate complement. The result is fever, rash, and arthralgias.
submitted by curlycheesefriesguy(5)
According to FA 2019, in the section about rheumatoid arthritis, it is given that rheumatoid nodules are due to fibrinoid necrosis. In the pathology chapter in FA, fibrinoid necrosis is said to be an example of type 3 hypersensitivity reaction. In this question stem, the patient is said to have rheumatoid nodules and they ask 'the immunologic mechanism of this patient's inflammation is similar to?' So basically they asked about what type of hypersensitivity reaction is fibrinoid necrosis. The answer: Rheum nodules->fibrinoid necrosis->type 3 HSR->same as serum sickness. Got it wrong btw.