The function of the immune system is to keep contagious microorganisms, such as definite bacteria, viruses and fungi, out of the body, and to demolish any infectious microorganisms that do attack the body. The immune system is completed by a complex and imperative network of cells and organs that guard the body from infection (1). The organs of the immune system are called the lymphoid organs, which have an effect on growth, development, and the free of lymphocytes (a confident type of white blood cell) (2). The lymphatic vessels and blood vessels are main parts of the lymphoid organs, because they transmit the lymphocytes to different areas in the body and from different areas in the body. All lymphoid organs play a task in the making and also activation of lymphocytes.

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Layered Defense
Organisms are protected by the immune system from infections with layered defenses of rising specificity. If these barriers were breached a pathogen, the innate immune system provides an immediate, but non-specific reaction. All plants and animals have Innate immune systems (3). If pathogens effectively evade the innate response, vertebrates have a third layer of protection, the adaptive immune system. The innate response activates the adaptive immune system.
Surface Barriers
The body of the human continuously faces attack from foreign invaders that can cause disease and infection. These invaders sort from living microbes , such as fungi, bacteria, parasites, and viruses, to dead toxins, drugs, and chemicals. As our luck, the body has many internal and external defenses that avoid most dangerous attackers from entering and causing damages. The physical layers that stay them at inlet commonly are referred to as the body’s 1st line of defense. The largest body organ is skin; is presents both a physical and also a chemical barrier against the outer environment. The skin makes a defensive cover that completely encloses around the body, shielding blood vessels, muscles, nerves, bones and organs. When tears or cuts in the outer surface of the skin, present an opening for infective organisms, glands under the skin, produce an enzyme that helps to destroy bacteria (4). Although areas of the body not covered with skin, do not unprotected. Mucous membranes, the wet layer of the respiratory system. They produce mucus, a sultry substance that catches irritants that enter through the nose.
Innate immune system
The cells that mediate immunity embody neutrophils, macrophages, and natural killer (NK) cells, giant lymphocytes that are not T cells but are cytotoxic. all these cells answer macromolecule and saccharide sequences distinctive to microorganism cell walls and to alternative substances characteristic of growth and transplant cells. They exert their effects by means of the complement and alternative systems, with the cells they attack oftentimes dying by osmotic lysis or cell death (5). Their cytokines also activate cells of the nonheritable immune system. a vital link in immunity in Drosophila melanogaster is a receptor supermolecule named toll, that binds plant life antigens and triggers activation of genes cryptography for antifungal proteins (6).
Humeral and Chemical Barriers
Some microbes penetrate the body’s protecting barriers and enter the interior tissues. There they encounter a variety of chemical substances which will stop their growth. These substances embody chemicals whose protecting effects are related to their primary perform within the body, chemicals whose principal perform is to harm or destroy invaders, and chemicals made by present bacterium (7).
Inflammation
Inflammation is one in every of the primary responses of the immune system to infection. The symptoms of inflammation are redness, swelling, heat, and pain, that are caused by augmented blood flow into tissue. Inflammation is made by eicosanoids and cytokines, that are released by livid or infected cells (6). Eicosanoids embody prostaglandins that manufacture fever and the dilation of blood vessels associated with inflammation, and leukotrienes that attract bound white blood cells (leukocytes). Common cytokines embody interleukins that are chargeable for communication between white blood cells; chemokines that promote chemo taxis; and interferon’s that have anti-viral effects, like motion down supermolecule synthesis within the host cell. Growth factors and cytotoxic factors may additionally be released (7). These cytokines and alternative chemicals recruit immune cells to the site of infection and promote healing of any broken tissue following the removal of pathogens.
Complement System
The complement system is a organic chemistry cascade that attacks the surfaces of foreign cells. It contains over twenty completely different proteins and is called for its ability to “complement” the killing of pathogens by antibodies. Complement is that the major humeral element of the innate response. several species have complement systems, as well as non-mammals like plants, fish, and some invertebrates (8),(9).
Cellular Barriers
Leukocytes (white blood cells) act like independent, acellular organisms and are the second arm of the innate immune system. The innate leukocytes embody the phagocytes (macrophages, neutrophils, and nerve fibre cells), mast cells, eosinophils, basophiles, and natural killer T cells. These cells identify and eliminate pathogens, either by attacking larger pathogens through contact or by engulfing so killing micro organisms (10).
Adaptive immune system
Lymphocytes are available in 2 major types: B cells and T cells. The peripheral blood contains 20-50% of current humorocytes; the rest move within the lymph system. Roughly eightieth of them are T cells, V-day B cells and remainder are null or undifferentiated cells. Lymphocytes constitute 20-40% of the body’s WBCs (6).
Their total mass is concerning an equivalent as that of the brain or liver. (Heavy stuff ) B cells are made within the stem cells of the bone marrow; they manufacture protein and superintend humeral immunity. T cells are non antibody-producing lymphocytes that are also made within the bone marrow but hypersensitised within the thymus and constitute the idea of cell-mediated immunity. the assembly of these cells is diagrammed below. parts of the immune system are changeable and may adapt to raised attack the invasive matter (11). There are 2 fundamental adaptive mechanisms: cell-mediated immunity and humeral immunity.
Lymphocytes
A white blood cell is a style of white corpuscle present within the blood. White blood cells help defend the body against diseases and fight infections. when the overall defense systems of the body have been penetrated by dangerous invasive microorganisms, lymphocytes help give a particular response to attack the invasive organisms (12).
Killer T cells
A large differentiated t cell that functions in cell-mediated immunity by attacking and essential amino acid target cells that have specific surface antigens (6). also known as cytotoxic t cell, killer cell.
Helper T cells
Any of varied T cells that, when stirred up by a particular matter, unharness lymphokines that promote the activation and function of B cells and killer T cells (13).
B Lymphocytes and Antibodies
A b cell identifies pathogens when antibodies on its surface bind to a particular foreign matter. This antigen/antibody advanced is preoccupied by the b cell and processed by chemical process into peptides. The b cell then displays these substance peptides on its surface MHC category II molecules (14). this combination of MHC and matter attracts a matching helper t cell, that releases lymphokines and activates the b cell. because the activated b cell then begins to divide, its offspring (plasma cells) secrete scores of copies of the protein that recognizes this matter (12). different adaptive immune system
The alternative adaptive immune systems in vertebrates have several similarities, but dissent therein Lucien-rich-repeat (LRR)-based variable white blood cell (VLR) receptors are employed by bone vertebrates versus the Ig-based TCR and BCR employed by jawed vertebrates. bone vertebrates have 2 VLR sorts, VLRA and VLRB, the various repertoires of that are expressed by separate lymphocytes populations (15).
Immunological Memory
the capability of the body’s immune system to recollect AN encounter with AN matter owing to the activation of B cells or T cells having specificity for the matter and to react more swiftly to the matter by means that of these activated cells during a later encounter (6).
Passive memory
Newborn infants have no prior exposure to microbes and are particularly prone to infection. many layers of passive protection are provided by the mother. throughout pregnancy, a selected style of protein, called IgG, is transported from mother to baby directly across the placenta, so human babies have high levels of antibodies even at birth, with an equivalent vary of matter specificities as their mother. Breast milk or colostrums also contains antibodies that are transferred to the gut of the baby and defend against microorganism infections until the newborn can synthesize its own antibodies (16).
Active memory
Long-term active memory is nonheritable following infection by activation of B and T cells. active immunity also can be generated by artificial means, through vaccination. The principle behind vaccination (also known as immunization) is to introduce AN matter from a microorganism in order to stimulate the immune system and develop specific immunity against that specific microorganism while not inflicting malady associated with that organism (17).
Disorders of Human Immunity
Some of the most devastating disorders which will affect the humanity are those that attack the very weaponry we’ve got against diseases, our immune system (7). These disorders can vary in severity from inflicting small rashes or a stuffy nose, to attacking important organs throughout the body, inflicting death. they can also come back from a variety of sources from the genetic passing down of traits, to infection from a malady. These immune system disorders comprise four categories: immunodeficiency, autoimmune, allergic and cancer.
Immunodeficiency
An immunodeficiency disorder is one in every of the many disorders that attack the immune system. In these disorders the immune system has problems that cause the system to not work correctly. again and again this can be owing to a genetic trait or congenital disorder (6). the most common immunodeficiency disorders are severe combined immunodeficiency (SCID), also known as “bubble boy” disorder, Di St. George syndrome, and ig A deficiency (18).
Motor vehicle Immunity
Autoimmune disorders attack the immune system by tricking the body into thinking its own organs are foreign invaders. when this happens, the phagocytes and lymphocytes activate healthy tissues and organs and destroy them. Common autoimmune diseases are lupus, scleroderma, juvenile dermatomyositis and juvenile rheumatism. The severity of AN disease can vary dramatically (19). Some could only cause localized swelling and inflammation by attacking the tissue within the joints, while others could cause death by attacking important organs.
Hypersensitivity
Hypersensitivity refers to excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions made by the traditional immune system. Hypersensitivity reactions need a pre-sensitized (immune) state of the host. Hypersensitivity reactions is divided into four sorts: type I, type II, sort III and kind IV, based on the mechanisms involved and time taken for the reaction (20).
Physiological Regulation
Hormones can act as immunomodulators, sterilisation the sensitivity of the immune system. as an example, female sex hormones are famous immunostimulators of both adaptive and innate immune responses. Some autoimmune diseases like autoimmune disease strike women preferentially, and their onset typically coincides with pubescence. in contrast, male sex hormones like testosterone seem to be immunosuppressive. alternative hormones appear to control the immune system yet, most notably luteotropin, endocrine and alimentation (21),(22).
Manipulation in medication
The response is manipulated to suppress unwanted responses ensuing from autoimmunity, allergy, and transplant rejection, and to stimulate protecting responses against pathogens that mostly elude the immune system (see immunization). immunosuppressive drugs are used to control autoimmune disorders or inflammation when excessive tissue harm occurs, ANd to stop transplant rejection once an transplantation. anti-inflammatory drug drugs are typically used to control the effects of inflammation. Glucocorticoids are the most powerful of these drugs; but, these drugs can have several undesirable facet effects, like central obesity, symptom, osteoporosis, and their use should be tightly controlled (23). Lower doses of anti-inflammatory drug drugs are typically used in conjunction with cytotoxic or immunosuppressive drugs such asmethotrexate or Imuran. Cytotoxic drugs inhibit the response by killing dividing cells like activated T cells. However, the killing is indiscriminate and alternative perpetually dividing cells and their organs are affected, that causes harmful facet effects. immunosuppressive drugs like cyclosporine stop T cells from responding to signals correctly by inhibiting signal transduction pathways (24).
What is dengue fever?
Dengue fever is a malady caused by a family of viruses that are transmitted by mosquitoes. it’s AN acute malady of sudden onset that typically follows a benign course with symptoms like headache, fever, exhaustion, severe muscle and joint pain, swollen glands , and rash.
Signs and Symptoms
Many folks, especially kids and teenagers, could expertise no signs or symptoms throughout a mild case of dengue fever. when symptoms do occur, they usually begin four to ten days once the person is bitten by AN infected dipteron (25).
Signs and symptoms of dengue fever most typically include:

Fever, up to 106 F (41 C)
Headaches
Muscle, bone and joint pain
Pain behind your eyes

You might also experience:

Widespread rash
Nausea and puking
Minor trauma from your gums or nose

Most people recover within per week or so. In some cases, however, symptoms worsen and may become grievous. Blood vessels typically become broken and leaky, and the number of clot-forming cells in your bloodstream falls (25). this will cause:

Bleeding from the nose and mouth
Severe abdominal pain
Persistent puking
Bleeding under the skin, which can appear as if bruising?
Problems along with your lungs, liver and heart

Clinical Course
The characteristic symptoms of breakbone fever are sudden-onset fever, headache (typically situated behind the eyes), muscle and joint pains, and a rash (25).
The alternative name for breakbone fever, “break-bone fever”, comes from the associated muscle and joint pains. The course of infection is split into 3 phases: febrile , critical, and recovery.
The febrile part involves high fever, typically over forty °C (104 °F), and is associated with generalized pain and a headache; this sometimes lasts 2 to seven days. At this stage, a rash occurs in 50-80% of those with symptoms. It occurs within the initial or second day of symptoms as flushed skin, or later within the course of malady (days 4-7), as a measles-like rash. Some petechiae (small red spots that do not disappear when the skin is pressed, that are caused by broken capillaries) can appear at this point, as could some gentle trauma from the secretion membranes of the mouth and nose. The fever itself is classically biphasic in nature, breaking so returning for one or 2 days, though there is wide variation in however typically this pattern truly happens (26).
Causes
Transmission
Dengue virus is primarily transmitted by Aides mosquitoes, particularly A. aegypti. These mosquitoes sometimes live between the latitudes of 35° North ANd 35° South below an elevation of 1,000 metres (3,300 ft). They bite primarily throughout the day. alternative genus Aedes species that transmit the malady embody A. albopictus, A. polynesiensis and A. scutellaris. Humans are the primary host of the virus, but it also circulates in anthropoid primates. AN infection is nonheritable via a single bite (27).
infectious agent Replication
Once inside the skin, breakbone fever virus binds to Langerhans cells . The virus enters the cells through binding between infectious agent proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins known as DC-SIGN, mannose receptor and CLEC5A. DC-SIGN, a non-specific receptor for foreign material on nerve fibre cells, seems to be the main purpose of entry. The nerve fibre cell moves to the nearest node (28). Meanwhile, the virus ordination is replicated in membrane-bound vesicles on the cell’s endoplasmic reticulum, wherever the cell’s supermolecule synthesis equipment produces new infectious agent proteins, and the infectious agent RNA is traced (26).
Severe malady
It is not entirely clear why secondary infection with a unique strain of breakbone fever virus places folks at risk of breakbone fever hemorrhagic fever and breakbone fever shock syndrome. the most wide accepted hypothesis is that of antibody-dependent enhancement (ADE). the exact mechanism behind ade is unclear. it may be caused by poor binding of non-neutralizing antibodies and delivery into the incorrect compartment of white blood cells that have eaten the virus for destruction. there is a suspicion that ade is not the only mechanism underlying severe dengue-related complications, and various lines of analysis have implied a role for T cells and soluble factors like cytokines and the complement system (25).
Diagnosis
Diagnosing dengue fever is tough, as a result of its signs and symptoms is easily confused with those of alternative diseases like malaria, swamp fever and enteric fever. Your doctor can seemingly raise concerning your medical and travel history. make sure to explain international visits thoroughly, as well as the countries you visited and the dates, yet as any contact you will have had with mosquitoes. bound laboratory tests can observe proof of the breakbone fever viruses, but test results sometimes come too late to assist direct treatment selections . (25),(27)
Classification
The World Health Organization’s 2009 classification divides dengue fever into 2 groups: uncomplicated and severe. The 1997 classification divided breakbone fever into undifferentiated fever, dengue fever, and breakbone fever hemorrhagic fever. breakbone fever hemorrhagic fever was divided additional into grades I-IV. Grade I is that the presence only of easy bruising or a positive bandage test in someone with fever, grade II is that the presence of spontaneous trauma into the skin et al, grade III is that the clinical proof of shock, and grade IV is shock so severe that pressure and pulse cannot be detected. Grades III and IV are noted as “dengue shock syndrome (27).
Prevention
All control efforts ought to be directed against the mosquitoes. it’s important to take control measures to eliminate the mosquitoes and their breeding places. Efforts ought to be intense before the transmission season and through epidemics (25),(27).
(1) stop dipteron bites:
(a) breakbone fever Mosquitoes Bite throughout the Daytime – defend Yourself from the Bite
(b) Wear full-sleeve clothes and long dresses to cover the limbs.
(c) Use repellents – care ought to be taken in victimisation repellents on young kids and elders.
(d) Use dipteron coils and electrical vapor mats throughout the daytime to stop breakbone fever.
(e) Use dipteron nets to safeguard babies, old folks et al who could rest throughout the day. The effectiveness of such nets is improved by treating them with permethrin. Curtains also can be treated with insecticide and decorated at windows or doorways, to repel or kill mosquitoes.
(f) Break the cycle of mosquito-human-mosquito infection. Mosquitoes become infected once they bite people that are sick with breakbone fever. dipteron nets and dipteron coils can effectively stop more mosquitoes from biting sick folks and help stop the spread of breakbone fever.
(2) stop the multiplication of mosquitoes:
Mosquitoes that spread breakbone fever live and breed in stagnant water in and around houses.
(a) Drain out the water from desert/window air coolers (when not in use), tanks, barrels, drums, buckets, etc.
(b) remove all objects containing water (e.g. plant saucers, etc.) from the house.
(c) All stored water containers ought to be unbroken lined in any respect times.
(d) Collect and destroy discarded containers within which water collects,
Treatment
There aren’t any specific treatments for dengue fever. Treatment depends on the symptoms, variable from oral rehydration therapy reception with shut follow-up, to hospital admission with administration of intravenous fluids and/or insertion. a decision for hospital admission is often based on the presence of the “warning signs” listed within the table on top of, especially in those with preexisting health conditions (27),(29).
Conclusion
Three immune parts interact to provide a confluence of symptoms that outline DHF/DSS. breakbone fever virus initially infects immature nerve fibre cells through the mediation of DC-SIGN. Infected nerve fibre cells contribute to pathological process through production of metalloproteases and cytokines (30). Downstream of nerve fibre cells T-cells become activated and generate the very cytokines concerned in tube-shaped structure leak and shock in addition to activating soul cells. protein enhancement is mediated by Fc receptors that are conspicuously on mature nerve fibre cells. infectious agent replication mediated by antibodies is increased 100-fold. in addition their effects on breakbone fever replication, antibodies to infectious agent epitopes cross react with cell a supermolecule that has the result of stimulating CD8 soul cells and production of cytokines and anaphylatoxins. Anaphylatoxins is generated directly through infectious agent proteins or through formation of AN antibody-complement advanced. Anaphylatoxins in turn can alter the reactivity of T-cells.