Immunology Flashcards
Second most common cause of severe combined immunodeficiency (SCID) and how does it cause the immunodeficiency?
Adenosine deaminase (ADA) [adenosine ⏩ inosine] deficiency ▶️ ⬆️ Adenosine ▶️ toxic to lymphocytes T and B
Which mechanism leads in a asplenic patient to have a severe bacterial infection? Immunologic functions of the spleen.
- 🚫 Systemic bacterial clearance ▶️ ⬆️ risk infections by encapsulated organism (vaccinate against S. pneumoniae, Hib, N. meningitidis)
- Blood filter ▶️ remove circulating pathogens; Major site of opsonizing antibody synthesis
What is the different between western blot and ELISA? And the similitude?
- Both identify proteins (Antibodies of the patient)
- ELISA ▶️ patient’s serum is tested directly (Ex look for Ab against some HIV proteins, or Ag as HBsAg)
- WB proteins are first separated by electrophoresis then the antibodies are added (in case to HIV test patient’s serum is added ▶️ Ex confirm that the Ab are specifically for the viral proteins directly extracted from the patient)
How is activated the classical complement pathway through C1?
C1 bind at least 2 different molecules of IgM or IgG ▶️ Fc portion near hinge region ▶️ C1 release catalytic factors for rest of pathway
How can you avoid the activation of classical complement pathway if no antigen is present?
Ag bind to IgM ▶️ expose region to bind C1; unbounded IgM hide C1 site binding ▶️ avoid activation without antigen.
Which enzyme is initially involved in ubiquitine proteasome pathway for the presentation of antigens in MHC type I? Function.
Ubiquitine ligase ▶️ recognize specific protein substrates and catalyze ubiquitine attachment
How do you identify a X-linked (Bruton) agammaglobulinemia and which is the gene mutated?
- Recurrent bacterial and enteroviral infections after 6 mo (⬇️ maternal IgG)
- Bruton tyrosine kinase gene (X-linked recessive) ▶️ maturation of B cells ▶️ stop until point to produce mu chain
- ⬇️Ig of all classes, ⬇️ peripheral CD19 cells, BM Bx ▶️ ⬆️ cells with cytoplasmic mu chains
What is the objective to administer anti-Rh(D) immunoglobulin to pregnant women? When is it applied?
- Anti-Rh(D) immunoglobulin (IgG anti-D, polyclonal Ab) ▶️ opsonize fetal RBC Rh (+) that enter to the maternal circulation ▶️ induce clearance by maternal reticuloendothelial macrophages (spleen) ▶️ avoid alloimmunization
- Give routinely all Rh (-) pregnancy at 28 weeks and immediately after birth
Recurrent skin and mucosal infections, without purulent secretion, absence of CD18 at leukocyte surface. Which other features do you find and what is the disease?
- Leukocyte adhesion deficiency→absence of CD18→no formation of functional beta-2 integrins
- Recurrent periodontal disease, persistent leukocytosis with neutrophilia, wound healing impaired and late separation of the umbilical cord (>21 days)
Classic triad of Reactive arthritis and with which genetic marker is associated?
- Nongonococcal urethritis (or enteritis) [1-4 weeks previously to next symptoms], conjunctivitis, oligoarthritis. 20% present sacroiliitis
- HLA-B27
*Seronegative spondyloarthropathy
Scenarios which graft vs host disease can develop. Background condition that allow the response and mechanism of disease.
- Bone marrow transplantation, transfusion of non-irradiated blood, organs rich in lymphocytes (as liver)
- Immunocompromised►primary disease or immunosuppressive medications→donor T cells from graft migrate into host tissues→recognize host MHC as foreigns→(+) CD4 and CD8 (no B cells)→host cell destruction
Most common organs affected by graft vs host disease.
- Skin→diffuse maculopapular rash with predilection by palms and soles (may desquamate)
- Liver→abnormal liver function tests (if transplant was liver, it could not be affected→recognized as self)
- GI tract→diarrhea, intestinal bleeding, abdominal pain.
In which background condition is the hyperacute rejection of a transplant developed?
Tissue recipient has antibodies against donor ABO antigens
*Minutes of transplantation→ischemia and necrosis
Substances resulting in degranulation of mast cells and basophils during anaphylaxis.
- Histamine
- Tryptase►specific of mast cells, ↑serum levels→support Dx of anaphylaxis (marker of mast cell activation)
How do you differentiate a cellular and humoral mediated acute transplant rejection reaction?
- Humoral→necrotizing vasculitis with a neutrophilic infiltrate, C4d deposition [Host B lymphocyte sensitization]
- Cellular→dense interstitial infiltrate of mononuclear cells (lymphocytes) and arterial intima (endothelitis) [Host T lymphocyte sensitization]
