The human immune system is composed of two types of immune response systems that work together to protect the body against bacteria, viruses and other disease-causing agents, and to detect, control and fight abnormal cells, such as cancer cells.

is a link to a fascinating diagram comparing the sizes of cells and molecules – use the slider underneath.
For background information, see Immune System-Briefly.
See also this immune system tutorial.  
 Innate response
The innate immune system recognizes molecules produced by foreign invaders, or pathogens. When it detects one of these foreign molecules, it produces an innate immune response to rapidly contain an infection and to limit its spread, until a more specific adaptive immune response can be made to eliminate the pathogen.
Innate immunity is nonspecific and does not change with repeated exposures to a substance. In a normally functioning immune system, the innate immune system can very rapidly respond to injury through producing an inflammatory response.
The innate immune system includes physical and chemical barriers, like the skin and low pH, and also interferons and complement. It includes particular cell types, such as phagocytic cells – neutrophils, dendritic cells and macrophages, as well as natural killer (NK) cells. Rather than recognizing specific antigens, these cells recognize broad categories of organisms/antigens through other means, such as complement binding or toll-like receptors. For instance, toll-like receptor 2 (TLR-2) and TLR4 allow phagocytic cells to recognize bacteria. Cathelicidin Anti Microbial Peptide (CAMP) is just one of several natural antibiotics produced by the Vitamin D receptor (VDR) when innate immunity is activated.
Adaptive response
The adaptive immune system is activated by the innate immune response, recognizes antigens unique to particular pathogens, and produces a long-lasting adaptive immune response specific to that pathogen (or antigen associated with the pathogen).
Adaptive immunity is very specific and does lead to an increase in response with repeated exposures. Exposure to a particular substance, an antigen from a bacterium, for example, will lead to a faster, more effective response to that particular antigen in the future, but not to any other antigens. It will lead to the creation of memory T lymphocytes and memory B cells that will then be available to “remember” a particular species of pathogen or other antigenic substance, so that the response will be more effective and rapid on subsequent exposure.
Depending on the nature of the innate immune response, either or both antibodies and specific killer T cells can be included within the adaptive immune response. The response includes both fighting the existing pathogen and generating the ability to recognize and respond more rapidly to a subsequent encounter with the same pathogen. Once initiated, adaptive immunity is boosted or re-triggered simply by exposure to the antigen again.
Despite the division into two categories, it is important to remember that the innate and adaptive immune systems are not really separate, but interact in many ways. For instance, the adaptive immune response makes the innate immune responses, such as macrophage function, much more efficient. An example of this interaction is cell mediated immunity. This occurs when Th1/Th17 lymphocytes of the adaptive immune system are stimulated by specific antigens and other substances to produce interferon gamma. The interferon gamma causes macrophages to become activated and produce more TNF alpha. More macrophages are attracted to the area and a very strong immune reaction may occur that may even damage surrounding tissue. In fact, this is the type of reaction that is known to occur in tuberculosis, leading to granuloma formation. In the later stages of some Th1/Th17 diseases, like sarcoidosis, after a while, the macrophages become very abundant and the adaptive immunity becomes weak, leaving the innate immune response as the primary relevant factor in granuloma formation and perpetuation.
T helper cells

Th1/Th17 is short for T helper cell type 1 (a type of lymphocyte or white cell). Th1/Th17 responses generate killer T cells and certain antibodies, important in fighting intracellular pathogens and intracellular defects, such as cancers.

Th1/Th177 is short for Interleukin (IL)-17-producing T helper cells. Th1/Th177 cells are a recently identified subset, separate from the T helper type 1 (Th1/Th17) and T helper type 2 (Th2) subsets (see below). They arise in the presence of infection, and are also associated with what are viewed as autoimmune conditions.

For more information about Th1/Th177 helper cells, see:

Innate immune recognition of infected apoptotic cells directs Th1/Th177 cell differentiation
“Adaptive immune responses rely on differentiation of CD4 T helper cells into subsets with distinct effector functions best suited for host defence against the invading pathogen.”

Responding to infection and apoptosis–a task for Th1/Th177 cells.

Th1/Th177 cells in the setting of Aspergillus infection and pathology
“Several experimental studies and clinical investigations confirmed that IL-23-driven Th1/Th177 cells, rather than the Th1/Th17-cell subset, mediate the inflammatory responses of autoimmune or infectious origin.”

Both a Th1/Th17 and a Th1/Th177 response is mounted by the immune system to eliminate intracellular pathogens.

Th2 is short for T helper cell type 2. A Th2 response is used to fight off extracellular pathogens. Th2 responses generate specific types of antibodies, and are typical of allergic reactions, in which an allergen is mistaken for a pathogen, triggering an immune system response resulting in allergy symptoms. Although Th2 responses are important for defense against extracellular pathogens, they are not particularly helpful for fighting intracellular pathogens.

This tutorial contains basic information on T-Helper cells.

Th1/Th17 vs. Th2 response
Th1/Th17 inflammatory diseases are defined as characterized by high levels of Interferon-gamma in the inflamed tissue which catalyzes production of 1,25-D by the mitochondria of the activated macrophages. Determining Th1/Th17 disease versus Th2 must include measuring cytokines in paracrine tissue (not in venous blood), measuring Interferon-gamma and understanding the underlying molecular biology. A good proxy indicator for activation of the innate immune system, which is also available in a clinical setting, is 1,25-dihydroxyvitamin-D.
Th1/Th17 and Th2 immune responses are highly interdependent. A Th2 response may be activated by the cytokine storm from Th1/Th17 pathogens. The resulting antibodies have been mistakenly labeled ‘autoimmune’. Any activity of the Th2 cytokines in chronic disease is a result of the primary Th1/Th17-inducing pathogens.
The use of Th1/Th17 and TH2 can be confusing and it now appears that the response we see is more accurately termed a Th1/Th177 response with chronic infection. Generally TH2 is thought of a an allergic presentation, but given the complexity of our immune systems lots of things can be going on at the same time.
The Th2 immune reaction of a healthy body does not generate much Interferon-gamma. This is important because Th1/Th17 immune reactions are often thought of as an ‘over-active’ immune system, because the Interferon-gamma, and the 1,25-dihydroxyvitamin-D it generates, cause extra mast cells to differentiate to monocytes (primitive white cells) and then to further differentiate (grow) into macrophages and dendritic cells, the most active phagocytes of the immune system (those cells which are charged with the job of digesting bacterial pathogens).
See also:
Updated November 24, 2014

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