This is the original historical table of 18 interleukins. Its scope, terminology and descriptions of immune function and treatments have not been reviewed for current scientific accuracy; blank cells remain blank as in the source.

Interleukins (also called lymphokines) are a sub-group of small soluable proteins called cytokines which function as chemical messengers between cells. The role of interleukins is to mediate and control the immunologic and inflamatory response. There are at least 18 known interleukins most of which have only been discovered in the last few years. Their role within the immune system is only beginning to be understood and they are just starting to be utilised in the treatment of a wide variety of diseases including cancer, AIDS and autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.

Interleukins are largely secreted by white blood cells (leukocytes) and received by receptors in others. The stimulation of interleukin receptors causes the recieving leukocyte to behave in a variety of ways depending on its type and the context. These include proliferating themselves, releasing other cytokines, inhibiting the release of other cytokines and activating themselves.

The interleukins are abbreviated to IL- followed by their number, eg. IL-2. Their receptors are suffixed with an "R" eg. IL-2R. The following table briefly describes the role of each of the known interleukins.

The role of the interleukins

_Interleukin_

Secreting cells

Action

Interleukin-1

IL-1

Macrophages

Stimulates T-cells to secrete interleukin-2 and activate the inflamatory response. It also causes the hypothalamus to increase the body temperature.

Interleukin-2

IL-2

Helper T-cells

Causes activated T- and B-cells to proliferate themselves. It also induces antibody synthesis.

Interleukin-3

IL-3

T-cells

Causes other leukocytes to be proliferated - it does this by making certain types of stem cell in the bone marrow to differentiate and grow. These stem cells (hematopoietic stem cells) mature into leukocytes.

Interleukin-4

IL-4

Helper T-cells

Causes T- and B-cells to grow. It's also a factor in the production of IgE antibodies.

Interleukin-5

IL-5

Helper T-cells

Stimulates B-cells, and eosinophils. It causes B-cells that produce IgA antibodies to proliferate

Interleukin-6

IL-6

T-cells,

Macrophages

Works in combination with alpha interferon to induce B-cell differentiation. It also causes the production of acute phase proteins in the liver and stimulates T-cells and other leukocytes.

Interleukin-7

IL-7

Stromal cells

Causes lymphoid stem cells to differentiate into progenitor T- and B-cells.

Interleukin-8

IL-8

Macrophages,

Endothelial cells

IL-8 is "sticky" for T-cells and neutrophils and helps to bring them to the site of an inflamation.

Interleukin-9

IL-9

Induces growth in in Helper T-cells.

Interleukin-10

IL-10

T-cells,

B-cells,

Monocytes,

Macrophages

Acts to inhibit some aspects of the immune system while stimulating others. It represses the production of other cytokines within the immune system, especially gamma interferon, TNF-alpha, IL-1 and IL-6. It inhibits antigen presentation but activates B-cells.

Interleukin-11

IL-11

Causes plasmacytoma cells to proliferate.

Interleukin-12

IL-12

Macrophages

Causes T-cells and Natural Killer cells to proliferate.

Interleukin-13

IL-13

T-cells

Promotes B-cell differentiation but inhibits inflammatory cytokine production.

Interleukin-14

IL-14

Dendritic cells,

T-cells

Enhances memory B-cell production and proliferation.

Interleukin-15

IL-15

Enhances T-cell proliferation in the blood.

Interleukin-16

IL-16

Acts as an adhesion molecule and activator for T-cells. Plays a part in both asthma and autoimmune diseases.

Interleukin-17

IL-17

T-cells

Activates neutrophils.

Interleukin-18

IL-18

Stimulates the release of Th1 cytokines.

Interleukin Links:

Interleukin

The Types And Functions Of InterLeukins In The Immune System

Interleukins

Interleukins: A group of bioactive proteins

Growth Factors and Cytokines

Source details

Author: Paul Jones

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