Host tropism is the infection specificity of certain pathogens to particular hosts and host tissues. This type of tropism explains why most pathogens are only capable of infecting a limited range of host organisms.

Researchers can classify pathogenic organisms by the range of species and cell types that they exhibit host tropism for. For instance, pathogens that are able to infect a wide range of hosts and tissues are said to be amphotropic. Ecotropic pathogens, on the other hand, are only capable of infecting a narrow range of hosts and host tissue. Knowledge of a pathogen's host specificity allows professionals in the research and medical industries to model pathogenesis and develop vaccines, medication, and preventative measures to fight against infection. Methods such as cell engineering, direct engineering and assisted evolution of host-adapted pathogens, and genome-wide genetic screens are currently being used by researchers to better understand the host range of a variety of different pathogenic organisms.

Research into AM functionality has been on the rise since AMs are one of the first lines of a defense against invasive pathogens. One of the most prominent fields is investigating liposomes as deliverers of antibiotics for treatment of respiratory intracellular infections. Intracellular parasites, such as M. tuberculosis, C. pneumoniae, L. monocytogenes, L. pneumophila, and F. tularensis, (to name a few) are taken up by AMs via phagocytosis, but are resistant to the biocidal mechanisms of AMs and can survive intracellularly, thus inducing severe respiratory infections. Pulmonary tuberculosis is caused by M. tuberculosis, and is now a major infectious disease worldwide and its incidence is increasing, especially in association with the AIDS pandemic. For sterilization of intracellular parasites in AMs, antibiotics are normally given orally or intravenously, but much of the antibiotics disperse to many different tissues, diminishing its effectiveness. Pulmonary administration of mannosylated liposomes is a much more direct, efficient route in targeting AMs; it enhances antimicrobial effect, reduces the dosage needed, and avoids unnecessary distribution to the blood. Since mannose receptors are exclusively expressed on the surface of AM, mannosylation of liposomes is an appealing approach to cell-selective targeting to AM. The efficacy of pulmonary administration of ciprofloxacin (CPFX) incorporated into mannosylated liposomes (mannosylated CPFX-lipososomes) was examined in rats, and determined to be an efficient means to target AMs.

Treatments used to combat autoimmune diseases and conditions caused by eosinophils include:

- corticosteroids – promote apoptosis. Numbers of eosinophils in blood are rapidly reduced

- monoclonal antibody therapy – e.g., mepolizumab or reslizumab against IL-5, prevents eosinophilopoiesis

- antagonists of leukotriene synthesis or receptors

- imatinib (STI571) – inhibits PDGF-BB in hypereosinophilic leukemia

Monoclonal antibodies such as dupilumab and lebrikizumab target IL-13 and its receptor, which reduces eosinophilic inflammation in pateints with asthma due to lowering the number of adhesion molecules present for eosinophils to bind to, thereby decreasing inflammation. Mepolizumab and benralizumab are other treatment options that target the alpha subunit of the IL-5 receptor, thereby inhibiting its function and reducing the number of developing eosinophils as well as the number of eosinophils leading to inflammation through antibody-dependent cell-mediated cytotoxicity and eosinophilic apoptosis.

This type of GvHD is associated with transfusion of un-irradiated blood to immunocompromised recipients. It can also occur in situations in which the blood donor is homozygous and the recipient is heterozygous for an HLA haplotype. It is associated with higher mortality (80-90%) due to involvement of bone marrow lymphoid tissue, however the clinical manifestations are similar to GVHD resulting from bone marrow transplantation. Transfusion-associated GvHD is rare in modern medicine. It is almost entirely preventable by controlled irradiation of blood products to inactivate the white blood cells (including lymphocytes) within.

Langerhans cells are dendritic cells (antigen-presenting immune cells) of the skin and mucosa, and contain organelles called Birbeck granules. They are present in all layers of the epidermis and are most prominent in the stratum spinosum. They also occur in the papillary dermis, particularly around blood vessels, as well as in the mucosa of the mouth, foreskin, and vagina. They can be found in other tissues, such as lymph nodes, particularly in association with the condition Langerhans cell histiocytosis (LCH).

There are a large number of clinical trials either ongoing or recently completed in the investigation of graft-versus-host disease treatment and prevention. Currently, there are no reliable molecular markers reflecting the onset or clinical course of aGVHD. However, it has been shown that genes responsible for cytokine signaling, inflammatory response, and regulation of cell cycle are differentially expressed in patinets with fatal GvHD versus „indolent“ GvHD.

On May 17, 2012, Osiris Therapeutics announced that Canadian health regulators approved Prochymal, its drug for acute graft-versus host disease in children who have failed to respond to steroid treatment. Prochymal is the first stem cell drug to be approved for a systemic disease.

In January 2016, Mesoblast released results of a Phase2 clinical trial on 241 children with acute Graft-versus-host disease, that was not responsive to steroids. The trial was of a mesenchymal stem cell therapy known as remestemcel-L or MSC-100-IV. Survival rate was 82% (vs 39% of controls) for those who showed some improvement after 1 month, and in the long term 72% (vs 18% of controls) for those that showed little effect after 1 month.

A pathogen will display tropism for a specific host if it can interact with the host cells in a way that supports pathogenic growth and infection. Various factors affect the ability of a pathogen to infect a particular cell, including: the structure of the cell's surface receptors; the availability of transcription factors that can identify pathogenic DNA or RNA; the ability of the cells and tissue to support viral or bacterial replication; and the presence of physical or chemical barriers within the cells and throughout the surrounding tissue.

Langerhans cells may be initial cellular targets in the sexual transmission of HIV, and may be a target, reservoir, and vector of dissemination.

Langerhans cells have been observed in foreskin, vaginal, and oral mucosa of humans; the lower concentrations in oral mucosa suggest that it is not a likely source of HIV infection relative to foreskin and vaginal mucosa.

On March 4, 2007 the online Nature Medicine magazine published the research letter "Langerin is a natural barrier to HIV-1 transmission by Langerhans cells." One of the authors of the study, Teunis Geijtenbeek, said that "Langerin is able to scavenge viruses from the surrounding environment, thereby preventing infection" and "since generally all tissues on the outside of our bodies have Langerhans cells, we think that the human body is equipped with an antiviral defense mechanism, destroying incoming viruses."

A lymphocyte is one of the subtypes of white blood cell in a vertebrate's immune system. Lymphocytes include natural killer cells (Phagocytes) (which function in cell-mediated, cytotoxic innate immunity), T cells (for cell-mediated, cytotoxic adaptive immunity), and B cells (for humoral, antibody-driven adaptive immunity). They are the main type of cell found in lymph, which prompted the name "lymphocyte".

Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route. Animals are also infected by "Y. pseudotuberculosis". The bacterium is urease positive.

Fumagillin has been used in the treatment.

Another agent used is albendazole.

Eosinophils, sometimes called eosinophiles or, less commonly, acidophils, are a variety of white blood cells and one of the immune system components responsible for combating multicellular parasites and certain infections in vertebrates. Along with mast cells and basophils, they also control mechanisms associated with allergy and asthma. They are granulocytes that develop during hematopoiesis in the bone marrow before migrating into blood, after which they are terminally differentiated and do not multiply.

These cells are eosinophilic or "acid-loving" due to their large acidophilic cytoplasmic granules, which show their affinity for acids by their affinity to coal tar dyes: Normally transparent, it is this affinity that causes them to appear brick-red after staining with eosin, a red dye, using the Romanowsky method. The staining is concentrated in small granules within the cellular cytoplasm, which contain many chemical mediators, such as eosinophil peroxidase, ribonuclease (RNase), deoxyribonucleases (DNase), lipase, plasminogen, and major basic protein. These mediators are released by a process called degranulation following activation of the eosinophil, and are toxic to both parasite and host tissues.

In normal individuals, eosinophils make up about 1–3% of white blood cells, and are about 12–17 micrometres in size with bilobed nuclei. While they are released into the bloodstream as neutrophils are, eosinophils reside in tissue They are found in the medulla and the junction between the cortex and medulla of the thymus, and, in the lower gastrointestinal tract, ovary, uterus, spleen, and lymph nodes, but not in the lung, skin, esophagus, or some other internal organs under normal conditions. The presence of eosinophils in these latter organs is associated with disease. For instance, patients with eosinophilic asthma have high levels of eosinophils that lead to inflammation and tissue damage, making it more difficult for patients to breathe. Eosinophils persist in the circulation for 8–12 hours, and can survive in tissue for an additional 8–12 days in the absence of stimulation. Pioneering work in the 1980s elucidated that eosinophils were unique granulocytes, having the capacity to survive for extended periods of time after their maturation as demonstrated by ex-vivo culture experiments.

Yersiniosis is usually self-limiting and does not require treatment. For severe infections (sepsis, focal infection) especially if associated with immunosuppression, the recommended regimen includes doxycycline in combination with an aminoglycoside. Other antibiotics active against "Y. enterocolitica" include trimethoprim-sulfamethoxasole, fluoroquinolones, ceftriaxone, and chloramphenicol. "Y. enterocolitica" is usually resistant to penicillin G, ampicillin, and cephalotin due to beta-lactamase production.

The primary method for controlling the incidence of gaffkaemia is improved hygiene. Other measures include limiting damage to the exoskeleton (preventing the bacterium's entry), reducing the water temperature, and reducing the stocking density. Antibiotics may be effective against the bacterium, but only tetracycline is currently approved by the U.S Food and Drug Administration for use in American lobsters.

In animals, "Y. pseudotuberculosis" can cause tuberculosis-like symptoms, including localized tissue necrosis and granulomas in the spleen, liver, and lymph nodes.

In humans, symptoms of Far East scarlet-like fever are similar to those of infection with "Yersinia enterocolitica" (fever and right-sided abdominal pain), except that the diarrheal component is often absent, which sometimes makes the resulting condition difficult to diagnose. "Y. pseudotuberculosis" infections can mimic appendicitis, especially in children and younger adults, and, in rare cases, the disease may cause skin complaints (erythema nodosum), joint stiffness and pain (reactive arthritis), or spread of bacteria to the blood (bacteremia).

Far East scarlet-like fever usually becomes apparent five to 10 days after exposure and typically lasts one to three weeks without treatment. In complex cases or those involving immunocompromised patients, antibiotics may be necessary for resolution; ampicillin, aminoglycosides, tetracycline, chloramphenicol, or a cephalosporin may all be effective.

The recently described syndrome "Izumi-fever" has been linked to infection with "Y. pseudotuberculosis".

The symptoms of fever and abdominal pain mimicking appendicitis (actually from mesenteric lymphadenitis) associated with "Y. pseudotuberculosis" infection are not typical of the diarrhea and vomiting from classical food poisoning incidents. Although "Y. pseudotuberculosis" is usually only able to colonize hosts by peripheral routes and cause serious disease in immunocompromised individuals, if this bacterium gains access to the blood stream, it has an LD comparable to "Y. pestis" at only 10 CFU.

Subcutaneous cysts may be surgically opened to remove less mature bots. If more matured, cysts may be opened and "cuterebra" may be removed using mosquito forceps. Covering the pore in petroleum jelly may aide in removal. If larvae are discovered within body tissues, rather than subcutaneously, surgical removal is the only means of treatment. Ivermectin may be administered with corticosteroids to halt larval migration in cats presenting with respiratory cuterebriasis, but this is not approved for use in cats. There is not yet a known cure for cerebrospinal cuterebriasis.

Although it is classified as a protozoal disease in ICD-10, their phylogenetic placement has been resolved to be within the Fungi, and some sources classify microsporidiosis as a mycosis, however, they are highly divergent and rapidly evolving.

There is usually an indication for a specific identification of an infectious agent only when such identification can aid in the treatment or prevention of the disease, or to advance knowledge of the course of an illness prior to the development of effective therapeutic or preventative measures. For example, in the early 1980s, prior to the appearance of AZT for the treatment of AIDS, the course of the disease was closely followed by monitoring the composition of patient blood samples, even though the outcome would not offer the patient any further treatment options. In part, these studies on the appearance of HIV in specific communities permitted the advancement of hypotheses as to the route of transmission of the virus. By understanding how the disease was transmitted, resources could be targeted to the communities at greatest risk in campaigns aimed at reducing the number of new infections. The specific serological diagnostic identification, and later genotypic or molecular identification, of HIV also enabled the development of hypotheses as to the temporal and geographical origins of the virus, as well as a myriad of other hypothesis. The development of molecular diagnostic tools have enabled physicians and researchers to monitor the efficacy of treatment with anti-retroviral drugs. Molecular diagnostics are now commonly used to identify HIV in healthy people long before the onset of illness and have been used to demonstrate the existence of people who are genetically resistant to HIV infection. Thus, while there still is no cure for AIDS, there is great therapeutic and predictive benefit to identifying the virus and monitoring the virus levels within the blood of infected individuals, both for the patient and for the community at large.

Because "B. suis" is facultative and intracellular, and is able to adapt to environmental conditions in the macrophage, treatment failure and relapse rates are high. The only effective way to control and eradicate zoonosis is by vaccination of all susceptible hosts and elmination of infected animals. The "Brucella abortus" (rough LPS "Brucella") vaccine, developed for bovine brucellosis and licensed by the USDA Animal Plant Health Inspection Service, has shown protection for some swine and is also effective against "B. suis" infection, but currently no approved vaccine for swine brucellosis is available.

An alveolar macrophage (or dust cell) is a type of macrophage found in the pulmonary alveolus, near the pneumocytes, but separated from the wall.

Activity of the alveolar macrophage is relatively high, because they are located at one of the major boundaries between the body and the outside world. They are responsible for removing particles such as dust or microorganisms from the respiratory surfaces.

Alveolar macrophages are frequently seen to contain granules of exogenous material such as particulate carbon that they have picked up from respiratory surfaces. Such black granules may be especially common in smoker's lungs or long-term city dwellers.

Inhaled air may contain particles or organisms which would be pathogenic. The respiratory pathway is a prime site for exposure to pathogens and toxic substances. The respiratory tree, comprising the larynx, trachea, and bronchioles, is lined by ciliated epithelia cells that are continually exposed to harmful matter. When these offensive agents infiltrate the superficial barriers, the body's immune system responds in an orchestrated defense involving a litany of specialized cells which target the threat, neutralize it, and clean up the remnants of the battle.

Deep within the lungs exists its constituent alveoli sacs, the sites responsible for the uptake of oxygen and excretion of carbon dioxide. There are three major alveolar cell types in the alveolar wall (pneumocytes):

- Type I pneumocyte (Squamous Alveolar) cells that form the structure of an alveolar wall.

- Type II pneumocyte (Great Alveolar) cells that secrete pulmonary surfactant to lower the surface tension of water and allows the membrane to separate, thereby increasing the capability to exchange gases. Surfactant is continuously released by exocytosis. It forms an underlying aqueous protein-containing hypophase and an overlying phospholipid film composed primarily of dipalmitoyl phosphatidylcholine.

- Macrophages that destroy foreign material, such as bacteria.

Type 1 and type 2 pneumocytes. Type 1 pneumocytes (or membranous pneumocytes) form the structure of the alveolus and are responsible for the gas exchange in the alveolus. Type 1 pneumocytes are squamous epithelial cells which are characterized by a superficial layer consisting of large, thin, scale-like cells; they also cover 95% of the alveolar surface, although they are only half as numerous as Type 2 pneumocytes. Type 2 pneumocytes are important in that they can proliferate and differentiate into type 1 pneumocytes, which cannot replicate and are susceptible to a vast numbers of toxic insults. Type 2 pneumocytes are also important because they secrete pulmonary surfactant(PS), which consists 80–90% of phospholipids [(phosophatidylcholine(PC), phosphatidyglycerol(PG), phosphaditylinositol (PI)] and 5-10% of surfactant proteins (SP-A, SP-B, SP-C, AND SP-D). PS is synthesized as lamellar bodies, which are structures consisting of closely packed bilayers that are secreted and then undergo transformation into a morphological form called tubular myelin. PS plays an important role in maintaining normal respiratory mechanics by reducing alveolar surface tension. By lowering alveolar surface tension, PS reduces the energy required to inflate the lungs, and reduces the likelihood of alveolar collapse during expiration. Loosely attached to these alveoli sacs are the alveolar macrophages that protect the lungs from a broad array of microbes and aerosols by devouring and ingesting them through phagocytosis.

Alveolar macrophages are phagocytes that play a critical role in homeostasis, host defense, the response to foreign substances, and tissue remodeling. Since alveolar macrophages are pivotal regulators of local immunological homeostasis, their population density is decisive for the many processes of immunity in the lungs. They are highly adaptive components of the innate immune system and can be specifically modified to whatever functions needed depending on their state of differentiation and micro-environmental factors encountered. Alveolar macrophages release numerous secretory products and interact with other cells and molecules through the expression of several surface receptors. Alveolar macrophages are also involved in the phagocytosis of apoptotic and necrotic cells that have undergone cell-death. They must be selective of the material that is phagocytized because normal cells and structures of the body must not be compromised. To combat infection, the phagocytes of the innate immune system facilitates many pattern recognition receptors (PRR) to help recognize pathogen-associated molecular patterns (PAMPs) on the surface of pathogenic microorganisms. PAMPs all have the common features of being unique to a group of pathogens but invariant in their basic structure; and are essential for pathogenicity(ability of an organism to produce an infectious disease in another organism). Proteins involved in microbial pattern recognition include mannose receptor, complement receptors, DC-SIGN, Toll-like receptors(TLRs), the scavenger receptor, CD14, and Mac-1. PRRs can be divided into three classes:

1. signaling PRRs that activate gene transcriptional mechanisms that lead to cellular activation,

2. endocytic PRRs that function in pathogen binding and phagocytosis, and

3. secreted PRRs that usually function as opsonins or activators of complement.

The recognition and clearance of invading microorganisms occurs through both opsonin-dependent and opsonin–independent pathways. The molecular mechanisms facilitating opsonin-dependent phagocytosis are different for specific opsonin/receptor pairs. For example, phagocytosis of IgG-opsonized pathogens occurs through the Fcγ receptors (FcγR), and involves phagocyte extensions around the microbe, resulting in the production of pro-inflammatory mediators. Conversely, complement receptor-mediated pathogen ingestion occurs without observable membrane extensions (particles just sink into the cell) and does not generally results in an inflammatory mediator response.

Following internalization, the microbe is enclosed in a vesicular phagosome which then undergoes fusion with primary or secondary lysosomes, forming a phagolysosome. There are various mechanisms that lead to intracellular killing; there are oxidative processes, and others independent of the oxidative metabolism. The former involves the activation of membrane enzyme systems that lead to a stimulation of oxygen uptake (known as the respiratory burst), and its reduction to reactive oxygen intermediates (ROIs), molecular species that are highly toxic for microorganisms. The enzyme responsible for the elicitation of the respiratory burst is known as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is composed of five subunits. One component is a membrane cytochrome made up of two protein subunits, gp91phox and p22phox; the remaining three components are cytosolic-derived proteins: p40phox, p47phox, and p67phox. NADPH oxidase exists in the cytosol of the AM when in a quiescent state; but upon activation, two of its cytosolic components, p47phox and p67phox, have their tyrosine and serine residues phosphorylated, which are then able to mediate translocation of NADPHox to the cytochrome component, gp91phox/p22phox, on the plasma membrane via cytoskeletal elements.

Compared to other phagocytes, the respiratory burst in AM is of a greater magnitude. Oxygen-independent microbicidal mechanisms are based on the production of acid, on the secretion of lysozymes, on iron-binding proteins, and on the synthesis of toxic cationic polypeptides. Macrophages possess a repertoire of antimicrobial molecules packaged within their granules and lysosomes. These organelles contain a plethora of degradative enzymes and antimicrobial peptides that are released into the phagolysosome, such as proteases, nucleases, phosphatases, esterases, lipases, and highly basic peptides. Moreover, macrophages possess a number of nutrient deprivation mechanisms that are used to starve phagocytosed pathogens of essential micronutrients. Certain microorganisms have evolved countermeasures which enable them to evade being destroyed by phagocytes. Although lysosomal-mediated degradation is an efficient means by which to neutralize an infection and prevent colonization, several pathogens parasitize macrophages, exploiting them as a host cell for growth, maintenance and replication. Parasites like Toxoplasma gondii and mycobacteria are able to prevent fusion of phagosomes with lysosomes, thus escaping the harmful action of lysosomal hydrolases. Others avoid lysosomes by leaving the phagocytic vacuole, to reach the cytosolic matrix where their development is unhindered. In these instances, macrophages may be triggered to actively destroy phagocytosed microorganisms by producing a number of highly toxic molecules and inducing deprivational mechanism to starve it. Finally, some microbes have enzymes to detoxify oxygen metabolites formed during the respiratory burst.

When insufficient to ward off the threat, alveolar macrophages can release proinflammatory cytokines and chemokines to call forth a highly developed network of defensive phagocytic cells responsible for the adaptive immune response.

The lungs are especially sensitive and prone to damage, thus to avoid collateral damage to type 1 and type II pneumocytes, alveolar macrophages are kept in a quiescent state, producing little inflammatory cytokines and displaying little phagocytic activity, as evidenced by downregulated expression of the phagocytic receptor Macrophage 1 antigen (Mac-1). AMs actively suppress the induction of two of the immunity systems of the body: the adaptive immunity and humoral immunity. The adaptive immunity is suppressed through AM’s effects on interstitial dendritic cells, B-cells and T-cells, as these cells are less selective of what they destroy, and often cause unnecessary damage to normal cells. To prevent uncontrolled inflammation in the lower respiratory tract, alveolar macrophages secrete nitric oxide, prostaglandins, interleukin-4 and -10(IL-4, IL-10), and transforming growth factor-β (TGF-β).

When infection attacks the body, "anti-infective" drugs can suppress the infection. Several broad types of anti-infective drugs exist, depending on the type of organism targeted; they include antibacterial (antibiotic; including antitubercular), antiviral, antifungal and antiparasitic (including antiprotozoal and antihelminthic) agents. Depending on the severity and the type of infection, the antibiotic may be given by mouth or by injection, or may be applied topically. Severe infections of the brain are usually treated with intravenous antibiotics. Sometimes, multiple antibiotics are used in case there is resistance to one antibiotic. Antibiotics only work for bacteria and do not affect viruses. Antibiotics work by slowing down the multiplication of bacteria or killing the bacteria. The most common classes of antibiotics used in medicine include penicillin, cephalosporins, aminoglycosides, macrolides, quinolones and tetracyclines.

Not all infections require treatment, and for many self-limiting infections the treatment may cause more side-effects than benefits. Antimicrobial stewardship is the concept that healthcare providers should treat an infection with an antimicrobial that specifically works well for the target pathogen for the shortest amount of time and to only treat when there is a known or highly suspected pathogen that will respond to the medication.

Viral entry is the earliest stage of infection in the viral life cycle, as the virus comes into contact with the host cell and introduces viral material into the cell. The major steps involved in viral entry are shown below. Despite the variation among viruses, there are several shared generalities concerning viral entry.

The three major types of lymphocyte are T cells, B cells and natural killer (NK) cells. Lymphocytes can be identified by their large nucleus.

Recent work has been done by virologists to learn more about the interference in infection of host cells and how DI genomes could potentially work as antiviral agents. The Dimmock & Easton, 2014 article explains that pre-clinical work is being done to test their effectiveness against influenza viruses. DI-RNAs have also been found to aid in the infection of fungi via viruses of the family "Partitiviridae" for the first time, which makes room for more interdisciplinary work.

"Y. enterocolitica" infections are sometimes followed by chronic inflammatory diseases such as arthritis, erythema nodosum, and reactive arthritis. This is most likely because of some immune-mediated mechanism.

"Y. enterocolitica" seems to be associated with autoimmune Graves-Basedow thyroiditis.

Whilst indirect evidence exists, direct causative evidence is limited,

and "Y. enterocolitica" is probably not a major cause of this disease, but may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.

"Y. enterocolitica" infection has also been suggested to not be the cause of autoimmune thyroid disease, but rather is only an associated condition, with both having a shared inherited susceptibility.

More recently, the role for "Y. enterocolitica" has been disputed.