TUTORIAL REPORT SGD 6 LBM 2 MODULE 3.

“THE MUCOSAL IMMUNE SYSTEM”

Group members :

Cahya Ardi Firjatullah (31102200026)

Diana Agustin (31102200035)
Fachrial Ikhsan (31102200039)
Indah Dwi Wahyu Ningsih (31102200059)

Kananta Kris Ananda (31102200068)

Laura Widya Safitri (31102200073)
Nasywa Windy Safithri (31102200098)
Nur Rahma Helmina Hikmah (31102200104)

Sandi Wahyu Pratama (31102200119)

Syifa Yudha Ardhiningrum (31102200129)

FACULTY OF DENTISTRY

SULTAN AGUNG ISLAMIC UNIVERSITY

 SEMARANG

2023

CONSENT SHEET

MODULE TUTORIAL REPORT

3.1 SGD 6 LBM 3

“The mucosal immune system”

Has been Approved by:

TUTORS LEADER

Drg. Eko Hadianto, MDSc Cahya Ardi Firjatullah

 Table of Contents

INTRODUCTION..........................................................................................................................4

A. Background.........................................................................................................................4

B. Scenario...............................................................................................................................5

C. Identification Of Problems..................................................................................................5

Literature Review.......................................................................................................................... 6

A. Theoretical Basis................................................................................................................ 6

1. The Mucosal Immune System Maintain Immunological Homeostasis........................... 6

2. The Anatomy In Gastrointestinal And Respiratory Tract................................................7

3. Kind And Mechanism Of Oral Cavity Immunity...........................................................11

Closing...........................................................................................................................................15

A. Conclusion......................................................................................................................15

Bibliography................................................................................................................................. 16
 CHAPTER 1
INTRODUCTION

A. BACKGROUND

All living organisms, from bacteria to humans, have evolutionary strategies for fighting infections from parasites. In
higher organisms, diversity and many strategies are also found in defense against parasitic microbes which are based
collectively on the immune system. The immune system in mammals consists of two types of interrelated immune
systems, namely the natural immune system (innate) and the adaptive immune system. The combination of innate and
adaptive systems allows the mammalian immune system to recognize and eliminate pathogen invasion with maximum
efficacy with minimal damage. This combination is also good for providing protection from re-infection by the same
pathogen. The innate and adaptive immune systems use 2 fundamentally different strategies to recognize specific
microbial invasions. The innate immune system detects infections using receptors that code for a limited number of
pathogens,and recognizing unique molecular structures to classify infectious microbes. The adaptive immune system
uses receptors randomly, and is highly specific with seemingly unlimited specificity. The combination of these two
recognition strategies is what makes the immune system in mammals so powerful.

In the adaptive immune system there are also two mechanisms, namely the humoral immune response mediated by
antibodies produced by B lymphocyte cells (or what are usually called B cells). Antibodies will recognize microbial
antigens, neutralize them, and eliminate the microbes using various effector mechanisms. Antibodies are specific
(only eliminate the antigen targets they recognize). Different types of antibodies can activate different effector
mechanisms. Cell-mediated immunity is mediated by T cells (T lymphocytes) which play a role in destroying cells
infected with microbes intracellularly (Shoemaker et al, 2001).

Iwama and Nakanishi (1996) broadly divided the body's defense (immune) system in fish into two, namely: the
nonspecific immune system and the specific immune system. Each immune system is further divided into immune
systems, namely cellular and humorous.
 B. SCENARIO

As the parasite attacks the host, the two come into a close dynamic
interaction. While the parasite tries to establish itself in/or the body of
the host, the host mounts a series of immune defensive actions against
the parasite. The outcome of these two actions depends on the degree
to which they are effective- the stronger wins over easily

C. IDENTIFICATION OF PROBLEMS
1. how the host mounts a series of immune defensive action against the parasite?

2. how to make the immune system more effective fight parasites

 CHAPTER 2
LITERATURE
REVIEW

A. THEORETICAL BASIS

1. how the host mounts a series of immune defensive action against the
parasite?

The innate host defense pathways consist of microbial sensors, their signaling pathways, and the effector
mechanisms they induce. The effector mechanisms fall into three broad categories: inflammatory
mediators, antimicrobial effectors, and signals inducing adaptive immune responses.

 Interactions of Host Defense Pathways

In principle, host defense pathways can engage in three types of interactions:
cooperation, complementation, and compensation
 A. Cooperation can be defined as the type of interaction where two (or more) individual
pathways optimally induce the same effector mechanism when both pathways are activated
(Figure 1A).
B. Complementation is a type of interaction where individual pathways activate distinct effector
mechanisms, which complement each other to form a functional unit of defense (Figure 1B). An
example of complementation is the interaction between the antibodies and phagocytes: both
effectors can function independently, but can complement each other to form a functional unit
of antibody-mediated phagocytosis.
C. Compensation is a type of functional interactions that occurs when one of the host defense
pathways is inactivated (for example, due to a mutation) while the other pathway(s) inducible by
the same infection remain intact. Compensation can be of two types depending on whether it
occurs at the level of sensors or effectors (Figure 1C). Thus, two sensors can compensate for
each other if they can both activate the same effector mechanism (Figure 1C, top). Alternatively,
two sensors may activate distinct effector responses, but if these responses are individually
sufficient to have a given effect (such as host protection), they will compensate for each other
(Figure 1C, bottom).

 Immune Compensation and Susceptibility to Infections

When a particular host defense pathway is disabled by mutations, as happens in experimental
animals and immunodeficient patients, infection susceptibility will depend on whether the defect
can be compensated for by the remaining pathways (Figure 2). If pathogen Px can be detected by
two sensors, A and B, that can both activate a protective effector response, inactivation of
pathway A (due to mutation or by pathogen e vasion mechanisms) can be compensated by
pathway B and the host will remain resistant to pathogen Px (Figure 2A). However, the same host
can be susceptible to pathogen Py that is detected by pathway A only (Figure 2B). A clinical
outcome of immunodeficiency in pathway A would be susceptibility to pathogen Py but not Px
and the incorrect conclusion would be that pathway A plays a role in defense against pathogen Py
but not Px. The correct interpretation of the same clinical observation, however, is that pathway B
can compensate for a defect in A in response to Px but not Py because Py does not activate
pathway B.
 In the second type of compensation, pathogen Px is detected by two pathways, A and B, that
activate distinct effector mechanisms: EM1 and EM2, respectively. When pathway A is
inactivated, the host will be protected from pathogen Px if EM2 is sufficient for protection
(Figure 2C) and susceptible to pathogen Py if EM2 is insufficient (Figure 2D). Patients with
pathway A mutation would be protected from pathogen Px and susceptible to pathogen Py. This
clinical presentation may lead to an incorrect conclusion that sensor A is irrelevant for protection
from Px when in fact a defect in A is compensated by EM2. If Px can evade recognition by sensor
B, however (Figure 2C), the outcome will be that sensor A is critical for protection from Px.

 Consequences of Immune Compensation

It should be noted that a compensatory increase in pathway B, when pathway A is disabled,

can lead to an incorrect interpretation that the mutated gene from pathway A plays a negative
regulatory role in pathway B. Finally, the compensatory enhancement of pathway B can be
caused not only by genetic immunodeficiency in pathway A, but also by evasion of genetically
intact pathway A by a pathogen.

 Redundancy in Host Defenses

In this scenario, B would be redundant when A is intact. However, if B has other functions,
such as activation of EM2, this additional function will maintain B if there is a selective
pressure to preserve EM2. Thus, A and B are redundant upon infection with pathogen Px that
can be detected
 by both A and B, but not during an infection with the pathogen Py that can only be detected by the sensor
B. Whether sensor B is essential or redundant would also depend on which pathogen Px or Py is more
common (see below). Clearly, the most common pathogens are the components of normal microbiota—
the opportunistic pathogens that cause overt infection only in immunocompromised humans and animals.
Thus, a key issue concerning the role of different host defense pathways in protection from infections is
the exposure rate to different types of pathogens, an issue that is not commonly considered in the analysis
of immunodeficiencies.

2. how to make the immune system more effective fight parasites

Of course, by improving our immune system so that it can be effective in fighting

parasites. Due to the nature of the parasite itself, namely hitching a ride on its
host's cells, in recent years these parasites have even been able to evade the
host's immune response. Therefore, the way to make our immune system more
effective is to improve our immune system through vaccination and maintaining a
healthy lifestyle by exercising and eating food that is not contaminated with
oocysts (T. Gondii)

• The immune system plays a crucial role in defending the body against parasites.
Here are a few tips:

1. Maintain a healthy lifestyle: Eating a balanced diet rich in fruits and vegetables,
exercising regularly, getting enough sleep, and maintaining a healthy weight can
help support your immune system

2. Avoid harmful substances: Limiting alcohol consumption and avoiding smoking or

drug use can help maintain a healthy immune system.

3. Practice good hygiene: Washing your hands regularly, especially before eating or
preparing food, can help prevent infections.

4. Avoid close contact with sick individuals: Parasitic infections can spread through
close contact with infected individuals.

5. Cook food thoroughly: Properly cooking food can help kill parasites and prevent
infections.
6. Stay hydrated: Drinking enough water helps maintain overall health and supports
the immune system.
B. CONCEPTUAL FRAMEWORK
 CHAPTER 3

CLOSING

A parasite is an organism that lives on or inside a host, taking resources from the host for its own survival. Parasites
are an important part of the ecosystem, but they can also cause disease in the host. Parasites can cause various health
problems in humans, animals and plants. They can cause serious illness, disrupt the function of the host organism, or
even cause death.
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