Question

Immunology Question

May you check my answers for 2a and 2b and see if: the information is being accurately presented, there is no unneeded information, and most importantly it is answering the question? I added more information to strengthen my answer so hopefully, it is better this time around. Thank you in advance!

2) Candida albicans is an opportunistic fungal pathogen in humans, and can cause a few irritating, but non- life threatening, infections in healthy individuals. However, in immunocompromised or immunodeficient individuals, C. albicans infections can be much more severe and lead to organ failure or death. Of note, individuals who are defective or deficient in any of the following suffer the worst candidiasis infections: macrophage function, expression of IFN-gamma, CD4+ T cells. a) Outline a mechanism to explain how Candida infections are normally controlled by these immune factors. Candida albicans, a common fungal human pathogen, triggers diseases from superficial mucosal to life- threatening systemic illnesses. This opportunistic pathogen is part of the human microflora that asymptomatically colonizes many areas of the human body where its proliferation is controlled by the host immune system. Under immune suppression conditions or interruption to the host environment, Candida an quickly turn into a pathogen and be able to cause infections. Candida albicans, as pathogens, adhere to host cell surfaces by the expression of adhesins. Adhesins are the agglutinin-like sequence (ALS) proteins which form a family consisting of eight members (Als1-7 and Als9). The ALS genes encode glycosylphosphatidylinositol (GPI)-linked cell surface glycoproteins. Of the eight Als proteins, the hypha- associated adhesin, Als3, is especially important for adhesion. Adhesion (along with physical forces and secretion of fungal hydrolases) can enable the second mechanism of invasion by destroying barriers in the host cells through fungal-driven active penetration (Tsui et al., 2016). The way this is done is, upon adhesion, these yeast cells form biofilms containing hyphal cells in its upper part and yeast cells in its lower. These biofilms allow increased resistance due to its intricate design, matrix, and enhanced expression of drug efflux pumps and metabolic plasticity. Several transcription factors control biofilm formation, which include the transcription factors Bcr1, Teci and Efgl. The biofilms of Candida albicans are resistant to killing by neutrophils and do not trigger production of reactive oxygen species (ROS). It is also evident that B-glucans in the extracellular matrix protect Candida albicans from these attacks (Tsui et al., 2016). Candida albicans would have grown hyphae during adhesion, therefore after adhesion this will allow secretion of hydrolases that are known to drive the fungal-driven active penetration. Candida albicans are expressed by three classes of hydrolases: lipases, phospholipases, and proteases, which will allow improvement of extracellular nutrient acquisition productivity. Candida albicans, besides metabolic flexibility, can prevent the creation of antimicrobial effectors and stimulate hyphal formation to avoid macrophages (Mayer et al., 2013). Macrophages are phagocytic cells that produce and release reactive oxygen species (ROS) in response to phagocytosis and so infections are said to be controlled. It was observed that killing of Candida albicans was linked with release of the ROS, superoxide, and granules. During this interaction HOCI generation occurred, one of the potent anti-fungal agents (Xu and Shinohora, 2017). A cytokine responsible for innate immunity and functions as the primary activator of macrophages, in addition to stimulating natural killer cells and neutrophils is Interferon gamma (IFN-Y). Host-fungi interactions lead to the production of IFN-y by host cells. IFN-Y plays an important role in the control of the infectious process, by direct activation of phagocytes, collaboration in the generation of protective antibody response, and favors the development of a Th1 protective response. IFN-y is produced by CD4, CD8, gamma delta T, and natural killer (NK) cells, essentially in response to both IL-12 and/or IL-18 cells by Candida albicans itself (Scriven et al., 2017).

Answer 1

The answer is to the point and mentions all the required information.

It is represented very well.

Please make sure you italicise or underline C. albicans where ever you mention it.

In part 2 b MPOD and LAD will also be responsible as they are also defects in immune system cells.

Kindly find appropriate information regarding these two defects.