Natural killer cells are sonamed because they are potent cytotoxic cells whose targets are not restricted i.e., they are not antigen-specific. They make up 5-10 percent of the  lymphocyte population.

They are activated by IL-15.

They have the appearance on light microscopy of large lymphocytes with numerous cytoplasmic granules and are sometimes called large granular lymphocytes. The granules contain substances that facilitate target cell lysis including perforin (a pore-forming protein) and granzymes. They classically express the CD16 and CD56 cell-surface markers.

NK cells attack virus-infected or abnormal cells expressing low levels of class I MHC molecules, while CD8+ T cells are MHC-restricted and attack cells with high level of class I MHC complexed to antigen.

NK cells insert perforin into the cells they are attacking and secrete granzymes through the pore. Granzymes attack the cell causing apoptosis.

NK cells can also kill cells through antibody-dependent cellular cytotoxicity where IgG bound to target cells interacts with Fc receptors (CD16) on NK cells causing release of lytic enzymes. NK cells are numerous in skin biopsies of patients with graft versus host disease following bone marrow transplant. They are also expanded in large granular lymphocyte (LGL) syndrome and in some patient with Felty’s syndrome.

mmune response can be segregated into four main types

Type I – IgE-mediated immediate hypersensitivity (e.g., allergic rhinitis or hayfever)
Type II – Antibody-mediated tissue injury, (e.g., autoimmune hemolytic anemia)
Type III –Immune complex (antigen-antibody) formation (e.g., serum sickness, Arthus skin reaction).
Type IV – Delayed-type hypersensitivity (e.g., immune response to mycobacterial antigens, positive PPD skin test)

MHC stands for major histocompatibility complex, a group of genes located on human chromosome 6. The products of MHC gene loci can be classified into two categories-class I and class II MHC molecules.

• Class I MHC molecules are expressed on the surface of all nucleated cells.

• Class II MHC molecules are found mostly on specialized cells called antigen-presenting cells.

Unlike macrophage, neutrophils, and B cells, T cells classically cannot recognize free soluble antigen. T cells can only “see” antigen via their surface T cell receptor, which will only bind to antigen bound to (“presented by”) an MHC molecule on the surface of a cell.

T cells “see” only pieces of large antigens because the antigen-binding groove in a MHC molecule can only accommodate a small peptide. Large protein antigens are digested (“processed”) prior to insertion in the groove.

An exception to the above involves stimulation of T cells by superantigens. A superantigen is typically a molecule of bacterial or viral origin that directly interacts with MHC class II molecules outside of the antigen-binding groove and then with the Vβ region in the T cell receptor.

The result is direct T cell activation of large amounts of T cells, all of which contain a specific Vβ region in the T cell receptor.

Therefore, the systemic host response to a superantigen can be substantial. Examples include toxic shock syndrome caused by a staphylococcal exotoxin that acts as a T cell superantigen.