Host immune system is the major barrier between pathogen and host. Resistance is the ability of an organism to defend itself from foreign substances/ pathogens.
There are various microorganisms that causes serious ailment in animals and humans like parasites are among them and they use various mechanisms to defend themselves from host body responses.
The parasites usually damage their host through different mechanisms and lead to damage. Among parasites, protozoa are the leading players. They can lead to acute and chronic infections. Protozoa damage the host through their cellular machinery, movement and by release of certain toxic products that lethally damage the host.
The parasites get in contact with immune system and they use certain mechanisms to escape immune system. They use escape mechanisms to avoid host and avoid getting killed.
There are some mechanisms that are used by parasites like antigen masking, through this they have ability to get avoided by immune system of host. They cover themselves with lost antigens.
Another renown mechanism is blocking of various factors, some parasites have a mechanism like they coat the antigen and antibody complexes and ultimately it blocks the binding of a specific antibody or WBC’s to surface antigens of parasites. Some parasites reside intracellularly, and it delays their detection by the immune system.
The major reason for vaccine development failure in parasites is their vast antigenic variation. They replicate their surface antigens and host immune system is unable to detect them. The parasites sometimes get advantage of immunosuppression of the host, so the ability of host immune system is reduced to detect or kill the parasite.
Types of Immune responses
There are different types of parasites that elicit different type of immune reactions. Either there is humoral immune response or cellular response. In plasmodium and Trypanosoma infections there is production of antibodies by the host immune system.
In Trypanosomiasis cytotoxic immune responses have been observed. The antibodies play key role in clearance of infection. The cellular immunity is major reason for resistance in case of malarial infection. There are various studies that have been published regarding antibody production against sporozoites.
Cytokines play role for both type of immune responses. Like in leishmaniasis, cellular immunity is important one as defense mechanism. The infection caused by toxoplasma gondii by usually taken over by macrophages. They play role in resistance. T cells are responsible for production of different cytokines. There is interferon (IFN-α) and interleukin-2 (IL-2) both are involved in cell mediated immune response. T-h1 cells produce IFN-g that is important in resistance against Leishmaniasis.
Type-2 helper cells have important role in parasitic infections and there is production of antibodies that is really important for development of resistance. These immune responses are usually downregulated by other immune cells. Because there is cascade of reactions that occurs in any kind of infection.
There is rise of one factor and another factor is downregulated by the uprising factor. These cytokines also influence other physiological mechanisms. There is influence on glucose, fatty acid and proteins metabolism. Interleukin and TNF- α causes increase in glucose oxidation and gluconeogenesis.
Cytokines can stimulate cell division process and also the of T and B cells. There are various pathological conditions that have been observed in parasitic infections. There are reactions among pathogen and host immune cells or pathogen and antibodies. Then these results in formation of immune complexes and these complexes circulate in host serum. Sometimes these complexes deposit in different organ systems like in kidneys.
Immunological complications in parasitic infections
The immune complexes formed in Trypanosoma and plasmodium infections. These complexes can be visualized using simple microscope in glomeruli of kidney. The cellular infiltration has also been observed. These infiltrates can cause glomerulonephritis in infected organisms.
The antigens of Trypanosoma have been observed in extravascular spaces. Antibody mediated autoimmunity has also been observed in parasitic infections. These is formation of autoantibodies and these are for host RBCs, laminin, DNA and collagen. These antibodies play their role in different ways, either they produce cytotoxic effects in host organ systems or there is formation of autoimmune complexes and these complexes deposit in different organ systems.
Hypersensitivity reactions have also been observed. These autoimmune responses are seen in some protozoal infections like Leishmania and Trypanosoma. There are cytotoxic lymphocytes that are responsible for auto-cytotoxic reactions in host.
These auto cells are harmful for host immune system. Cell mediated hypersensitivity has also been observed in protozoal infections. The lesions in Leishmaniasis are due to cell mediated response. The formation of granulomas is an example of autoimmunity in tuberculosis and schistosomiasis.
It has been observed that Tumor Necrosis factor may be involved in the muscle wasting condition that is seen in the chronic form of African trypanosomiasis. The immunosuppression is commonly seen in young children and old age people.
This phenomenon itself is pathologic. The people usually are immunosuppressed due to lots of factors. Sometimes it is seen that it is only due to host’s own system fault and also some to some parasitic infections like Malaria, Trypanosoma and Leishmania.
Sometimes it is due to proliferation of T suppressor cells or macrophages that inhibit the immune system by excreting of regulatory cytokines and production of specific immune system suppressing substances by the parasite. All these mechanisms are quite complex, and these are still understudy.
This article is jointly written by Hammad Ur Rehman Bajwa Department of Parasitology , Muhammad Kasib Khan Department of CMS, Arsalan Zafar Institute of Animal and Dairy Sciences, Muhammad Shafi Hasni, Nauman Iftikhar, and Muhammad Uzair Asghar.