M cells sample luminal antigens and deliver them to underlying immune cells

The mucosal immune system functions independently of epithelial cells 

Intraepithelial lymphocytes are absent from the intestinal epithelium 

Peyer’s patches are found only in the thymus

Secretory IgA is mainly a monomer without epithelial transport

Tumor-associated neutrophils (TANs) facilitate tumorigenesis in platelets, thereby triggering ITP

Extremely high platelet count

CD6+ T cells are activated during the onset of ITP

Antibody binding to various platelet surface structures, like gpIIb-IIIa integrin, makes them susceptible to opsonization and phagocytosis by splenic macrophages

PD-1 is expressed on the cell surface of platelets and is responsible for ITP

Retention of MHC I in the cell

Increasing the expression of MHC I molecules on the cell surface

Secretion of a protease to degrade IgA dimers

Inhibition of phagosome-lysosome fusion

Blocking the TAP transporter in the ER

The treatment results in an increase in autoimmunity

The treatment increases the risk of infection

The treatment provokes a septic shock

There are no side effects

The treatment increases the risk of only lung cancer

Differentiation of B cells to plasma cells

Molecular mimicry

Antigenic drift

Degradation of restriction factors

Downregulation of MHC I molecules

It is mediated exclusively by CD8+ T cells

Histamine has no role in vascular permeability

It depends on IgG but not IgE

Mast-cell degranulation is triggered when an allergen cross-links IgE bound to FcεRI

Eosinophils are never involved in allergic inflammation

Produced by plasma cells that are directed against foreign receptors 

Produced by plasma cells that are directed against “self-receptors” and “self-proteins”

Secreted by all antigen-presenting cells that are directed against our own body's receptors and cells

Responsible for binding self-antigens, but only with their Fc part

Produced by basophils that are directed against enemy receptors and cells

Insulin receptor only

Integrins on platelets only

Nuclear antigens such as DNA, histones, and ribonucleoproteins

Acetylcholine receptor only

Thyroid-stimulating hormone receptor only

Alteration in the self-protein status in the body

Cross-reaction with antibodies with their Fc part to a foreign antigen

The use of broad-spectrum antibiotics

Mutations in cytokine IL-123 delivery

A defect in T regulatory cell function

Effector mechanisms in autoimmunity include circulating high-affinity antibodies recognizing pathogens

Failure of self-tolerance results in immune against self-antigens and destruction of cells or normal tissue

All autoimmune diseases show higher incidence in males than in females

Among the genes associated with autoimmunity, coding for the CD4 molecule is the most affected gene

Infectious pathogens are present in all autoimmune lesions