Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
26 Cards in this Set
- Front
- Back
|
Engraftment of allogeneic tissue
|
Engrafted dendritic cells in implant initiate immune response (direct)
More significant |
|
|
Engraftment of allogenic tissue
|
Recipient dendritic cells process and present antigen to initiate immune response (indirect)
Less significant |
|
|
Engraftment of allogenic tissue
and Engraftment of allogeneic tissue lead to |
CD4+ helper cells
Humoral immunity (B cells) CD8+ cytotoxic T cells which leads to Vascular damage Tissue damage Antibody + C ADCC T cell killing Complement |
|
|
Hyperacute rejection (minutes to hours after graft)
|
Preformed antibodies against recipient antigens
Scenarios: prior transplants, pregnancy, prior blood transfusions Immediate attack of vasculature Immunoglobulin + complement in vascular walls Thrombotic occlusion of capillaries (ischemia-infarction) |
|
|
Acute cellular rejection (days to months)
|
Cellular infiltrates of CD4 and CD8 positive cells
Activated cell phenotypes Endothelial and epithelial damage Minimal or no fibrosis Responsive to T cell immunosuppressive drugs (cyclosporin) RECOGNIZE! The “inflammation” is chronic, but the rejection pattern is “acute”. |
|
|
Acute humoral rejection (induction of antibodies)
|
Necrotizing vasculitis
Slower progressive reduction in vascular patency yielding infarction Deposition of C4d component of complement (marker of complement activation by classical pathway) Responsive to B cell depletion |
|
|
Chronic rejection (months to years)
|
Obliterating intimal fibrosis (vascular)
Parenchymal fibrosis Slow loss of blood supply Parenchymal atrophy or cellular loss Progressively declining function |
|
|
Graft versus host disease
|
Transplantation of competent immune cells from donor to immunoincompetent recipient; Donor rejection of recipient’s tissue
|
|
|
Graft versus host disease
Two Scenarios |
Acute graft versus host disease
Primarily affects skin, liver, intestine Chronic graft versus host disease Predominantly skin, but also liver, intestine Decimated immune system with opportunistic infections |
|
|
Interventions of Immunosuppression
|
Cyclosporine: Blocks T cell activation at transcription factor NFAT, abrogating cytokine response. Cell focused.
Azothioprine: inhibits leukocyte production Steroids: block or reduce inflammation Inhibitors of lymphocyte proliferation (rapamycin) Antibodies against cellular subsets or receptors (anti-TNFα antibodies, others). |
|
|
Immune Deficiency Disease Primary
|
Usually genetic defect
Targets specific components of the immune system, cells of the immune system, or proteins in cells of the immune system |
|
|
Immune Deficiency Disease Secondary
|
Acquired forms of immunodeficiency
Prototypic disease is HIV infection Other types of induced immunodeficiency (mostly viral infections that may damage immune system) |
|
|
Immune Deficiency Disease (iatrogenic
|
Drug- or treatment-induced
|
|
|
Primary Immunodeficiency X-linked Agammaglobulinemia big pic
|
No B cells
No plasma cells Follicular hypoplasia |
|
|
Primary Immunodeficiency X-linked Agammaglobulinemia
|
Mutation in Bruton’s tyrosine kinase
Protein required for B cell maturation via Ig receptor complex Maturation stops at Pro-B; no light chain expression Clinical: recurrent infections (Haemophilus influenzae, Streptococcus pneumoniae, Staph aureus) What does the lymphoid profile look like? In blood? In lymph nodes and lymphoid tissues? Almost always boys, rarely girls |
|
|
Primary Immunodeficiency Common Variable Immunodeficiency and selective IgA deficiency
|
Heterogeneous group – many mechanisms
May be related to B cell or T cell malfunction Clinical expression related to antibody deficiency Problems at the interface to the environment (respiratory, gastrointestinal, urogenital) Association with autoimmune diseases |
|
|
Primary Immunodeficiency
|
Hyper-IgM syndrome
Lack of T cell help; no Ig class switching X linked (70%): CD40 ligand mutation on Xq26 Autosomal recessive (30%): CD40 mutation or enzyme defect (activation induced deaminase, a DNA editing enzyme required for class switch) Serum gamma globulin is all IgM |
|
|
Hyper-IgM syndrome
Serum gamma globulin is all IgM and causes |
Auto-reactive IgM antibodies develop (hemolytic anemia, thrombocytopenia, neutropenia)
Few or no opsonizing antibodies yield pyogenic infections |
|
|
Primary ImmunodeficiencyDiGeorge Syndrome
|
Failed development of 3rd and 4th pharyngeal pouches
No thymus – no T cells. No parathyroids – calcium abnormalities Altered facial structure Not familial. It is a 22q11 deletion. |
|
|
Primary Immunodeficiency Severe Combined Immunodeficiency
|
X-linked is deficiency of γ chain of cytokine receptors (50-60%). No cytokine signaling.
Autosomal recessive is a cluster of enzyme defects Adenosine deaminase most common Others specific defects |
|
|
Primary Immunodeficiency
|
Thrombocytopenia
Eczema Immunodeficiency |
|
|
Primary Immunodeficiency Complement receptor deficiencies
|
C1 inhibitor = Hereditary angioedema (fails to control C1r, C1s, Factor XII)
Alternative pathway components more important |
|
|
Amyloidosis
|
Many proteins, similar appearance and structure
β pleated sheets Several important types AL – composed of immunoglobulin light chains AA – part of SAA, a acute phase reactant protein; chronic inflammation Aβ in Alzheimers Disease – present in plaques and cerebral vessels |
|
|
Amyloidosis Invokes
|
pressure atrophy with buildup
Major malfunction when the glomerulus is involved. |
|
|
Amyloidosis Many disease associations
|
Immunocyte dyscrasias (myeloma, immunoglobulin light chains, AL type)
Reactive systemic amyloidosis (AA type) Hemodialysis associated (β2-microglobulin) Endocrine tumors (medullary carcinoma of thyroid) Senile amyloid (usually cardiac – transthyretin) Alzheimer disease (Aβ protein) |
|
|
Amyloidosis: many different proteins; one appearance
|
(hyalin)
|
