The innate immune system and the adaptive immune system each comprise both humoral and cell-mediated components.
Different animal species can be more or less resistant to specific pathogens.
Within a species, individual organisms may be more or less susceptible to a pathogen based on age, nutrition, stress, disease state, and chemicals in their environment.
Whether a pathogen can cause disease in a host is dependent not only on the virulence of the pathogen, but also on the genetic background and health of the host. Some species have an innate susceptibility to a pathogen not shared with other related hosts. For example, humans are the only host for the agents of syphilis, gonorrhea, measles and poliomyelitis. In contrast, we have innate resistance to canine distemper virus and feline leukemia virus. These differences in susceptibility may be related to a number of factors. The resistant host may lack a cellular receptor required by the pathogen for attachment or penetration of the host. The temperature of the host may also preclude the growth of a potential pathogen.
Individuals within a species can also exhibit different susceptibility or resistance to a pathogen when compared to others. The age of an individual can have an overall effect on disease resistance, with the very young and the very old being more susceptible to infection by a wide variety of pathogens. Stress in the form of extreme exertion, shock, a change in environment, climate change, nervousness or muscle fatigue can have a negative impact on health. Each of these conditions is thought to increase the release of cortisol from the adrenal cortex, causing a suppression of the inflammatory response, thereby facilitating infection.
1. Differences in susceptibility to certain pathogens
-Absence of specific tissue or cellular receptors for attachment (colonization) by the pathogen.
-Temperature of the host and ability of pathogen to grow.
-Lack of the exact nutritional requirements to support the growth of the pathogen.
-Lack of a target site for a microbial toxin.
2. Anatomical defense
The structural integrity of the body surfaces, i.e., the skin and mucous membranes, forms an effective barrier to initial lodgment or penetration by microorganisms. The skin is a very effective barrier to bacterium, so that no bacterium by itself is known to be able to penetrate unbroken skin. Of course, a puncture, cut or scrape in the skin could introduce infectious bacteria. The mucous membranes are more vulnerable to penetration by infectious bacteria but still pose a formidable barrier of mucus and antimicrobial substances.
The anatomical defenses are associated with all other aspects of non-cellular immunity, including individual resistance, mechanical resistance, chemical resistance and resistance established by the normal flora.
3. Tissue bactericides, including complement
4. Microbial antagonism
Microbial antagonism is the method of using established cultures of microorganisms to prevent the intrusion of foreign strains. When introduced to an already-colonized environment, an invasive strain of bacteria tends not to thrive and may go completely extinct.
These 4 can be considered as non-cellular defense.
5.Inflammation : Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.
and 6.Phagocytosis: specific form of endocytosis involving the vascular internalization of solids such as bacteria by an organism, and is therefore distinct from other forms of endocytosis such as the vesicular internalization of various liquids
5 &6 are forms of cellular defense.
Immune responses to antigens may be categorized as primary or secondary responses. The primary immune response of the body to antigen occurs on the first occasion it is encountered. Depending on the nature of the antigen and the site of entry this response can take up to 14 days to resolve and leads to the generation of memory cells with a high specificity for the inducing antigen. The humoral response, mediated by B cells with the help of T cells, produces high‐affinity and antigen‐specific antibodies. This is in contrast with the CD8 T‐cell response which leads to the generation of large numbers of antigen‐specific cells that are capable of directly killing infected cells. Antigen‐specific CD4 T cells, which provide help to B cells in the form of cytokines and other stimulatory factors, can also be expanded upon antigenic stimulation.
The secondary response of both B‐ and T cells is observed following subsequent encounter with the same antigen and is more rapid leading to the activation of previously generated memory cells. This has some quantitative and qualitative differences from the primary response.
The innate immune system is the first line of defence against infectious agents. When this is breached, the adaptive immune system provides a more efficient response to clearing pathogens. The adaptive immune system has the capacity to ‘remember’ previous antigens, a process termed immunological memory. Antigen‐specific T cells are selected during a primary immune response and expand to produce clones of T cells with high specificity for the activating antigen. In a B cell primary response to a thymus‐dependent antigen, the immune system selects B cells with a high affinity and specificity for the antigen and these become memory cells.The selection of B cells with a high affinity for a given antigen occurs in the germinal centers of secondary lymphoid follicles and requires the enzyme activation‐induced cytidine deaminase (AID) and interactions with other immune cells.The ability to change the isotype of antibody produced (class switching) by a B cell also occurs in germinal centers and requires AID. In a secondary response to the same antigen, memory cells are rapidly activated. This process is quicker and more effective than the primary response. Antibody-mediated beta cellularis immune system, is the aspect of immunity that is mediated by macromolecules (as opposed to cell-mediated immunity) found in extracellular fluids such as secreted antibodies, complement proteins and certain antimicrobial peptides. Humoral immunity is so named because it involves substances found in the humours, or body fluids.
Cell-mediated immunity is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cytotoxic T cells cause death by apoptosis without using cytokines, therefore in cell mediated immunity cytokines are not always present.
The statistical errors identified in Infection and Immunity are comparable to those found in similar journals: 54% of the articles reviewed contained errors of analysis (20%), reporting (22%), or both (12%). The most common analysis errors are failure to adjust or account for multiple comparisons (27 studies), reporting a conclusion based on observation without conducting a statistical test (20 studies), and use of statistical tests that assume a normal distribution on data that follow a skewed distribution (at least 11 studies). The most common reporting errors are unlabeled or inappropriate error bars or measures of variability (15 studies) and failure to describe the statistical tests performed (12 studies).
- Track 3-1Differences in susceptibility to certain pathogens
- Track 3-2Antibody-mediated Immunity
- Track 3-3Induction of a secondary immunological response
- Track 3-4Induction of primary immunological responses
- Track 3-5Phagocytosis
- Track 3-6Inflammation (ability to undergo an inflammatory response)
- Track 3-7Microbial antagonism
- Track 3-8Tissue bactericides, including complement
- Track 3-9Anatomical defense
- Track 3-10Cell-mediated Immunity