Immune system cells, called lymphocytes, use proteins called cytokines to communicate and induce an immune response. The lymphocytes known as helper T (Th) cells include several subtypes, including Th1 cells. Th1 cells are responsible for causing macrophages to attack invading organisms and infected cells. They use specific Th1 cytokines such as interferon-γ (INF-γ) and tumor necrosis factor-β (TNF-β) to accomplish these tasks.
Th1 cytokines have two main purposes. First, they recruit and activate nearby macrophages, which destroy invaders like bacteria. Macrophages will engulf other organisms, but will not digest them until told to do so by these cytokines. These cytokines will also signal other leukocytes to the site. The leukocytes will then begin the inflammatory response, increasing blood flow to allow other immune cells to reach the area.
The response created by the release of Th1 cytokines primarily induces other cells to neutralize invaders, so it is known as the cellular immune process. These cytokines affect cells called CD8+ T cells, yet another class of immune cell. CD8+ T cells eliminate tumor cells and cells infected by viruses. INF-γ and TNF-β causes these cells to increase, expanding the local immune response.
A useful function of Th1 cytokines is to increase the number of Th1 cells in the area. Helper T cells require the presence of interleukin-12 (IL-12) to become Th1 cells. The released INF-γ communicates with macrophages and dendritic cells in the area, and causes them to release IL-12. This, in turn, creates greater amounts of Th1 cells, causing them to release more INF-γ, in a feedback cycle.
Research has shown that these cytokines are essential for preventing the progression of certain diseases and conditions. Diseases such as malaria can impair the cellular immune response. Th1 cells that can continue to produce high levels of IL-12 and INF-γ tend to be successful in fighting this parasite. When organisms cannot create an effective Th1 response, malaria tends to switch from a mild form to one that can kill.
Some types of hypersensitivity, the underlying mechanism behind autoimmune diseases, are attributed to Th1 cytokines. Specifically, they are involved in delayed-type hypersensitivity, which is a slower, prolonged autoimmune response. An initial release of cytokines brings macrophages and other leukocytes to the area.
These cells, in turn, release other cytokines that encourage the presence of Th1 cells. The resulting feedback loop causes persistent inflammation and pain. Unlike other forms of hypersensitivity, delayed-type does not involve antibodies, so it is not an allergic response.