2.4.

Development of the humoral immune response :

2.4.1. MECHANISMS, GENERAL FUNCTIONS :

- There are no fundamental differences between mammals and birds

^ Helper T cells and MHC (major histocompatibility complex) occur in both birds and
mammals

^ Complement fixation in birds is as effective as in mammals

^ Birds have plasma cells (producing antibodies) with surface immunoglobulins with
a half live of 5-6 days (unlike mammals).

^ Birds have minor structural differences in immunoglobulins when compared to

mammals; IgG has a higher molecular mass than IgG and has the same level of
homology in the constant regions of both mammalian IgG and IgE.

There is some speculation that in mammals IgG and IgE come from a common precursor
and that division has not yet produced in the avian species.

Experimentally heterogeneity has been observed in IgG but only one constant gamma
region has been identified.

Corticosterone is the main cortical adrenal hormone in poultry; its lack of

immunosuppressive properties associated with other steroids has been speculated,
even in high doses.

However, this has not been proven true for chicken and may not apply to other
species.

The genes that encode the constant region of IgM and IgG are linked together; these
genes recombine at a rate of around 2%; this would be up to twice as large as
observed in mammals.

Blood IgA appears at 10 days of age and IgM at 4 days of age.

2.4.2. MATERNAL IMMUNITY:

The immunoglobulins IgM and IgA are present in the amniotic fluid and the ingestion
of this by the embryo at birth resembles the ingestion of colostrum in mammals.

The IgG (Y) are found in the yolk (yolk sac) that begins to be reabsorbed during
the first 24 hours after hatching; even during embryogenesis there are
an important concentration of antibodies in blood that have migrated through the
own circulation of the embryo that occurs during incubation and before hatching.

Poor incubation or failure of the yolk sac absorption may affect the transfer of
maternal immunity and in some cases the availability of nutrients.

The half-life of a chicken IgG during the first week

of life is twice as much as that of an adult, for
compensate for the time it takes to absorb the yolk sac (3-5 days).

The amount of circulating antibodies that are transferred from the hen to the chick
can vary with the age of the hen, the laying cycle, and also with the level or
titer of circulating chicken antibodies; the increase of the titre in the hen serum
will not necessarily induce an increase in the concentration of the antibodies in
the yolk (the increase of two-fold the titer in the serum will not increase the
titre in the yolk twice, rather it is expected a lower title).

Under commercial conditions the antibodies generated by

periodic vaccinations allow to estimate a transfer rate from the hen to the chick
of 70-80% according to the disease analyzed.

2.4.3.Local IMMUNITY:

The primary mediator of this type of immunity is IgA; Avian IgA is structurally
related in some to mammalian IgM but functions as mammalian IgA.

Avian IgA has the secretory component in all secretions except bile; the gA and IgG
heavy avian chains appear to have 4 domains of constant regions instead of 3.

Serum IgG is also very important.

The role of the Harderian gland in the local immunity of

Birds is unique but it is controversial; The extirpation of the gland has been
related to both the no effect and the decrease of local immunity.

Local immunity plays an important role in the protection against pathogens in the
respiratory system.

In the bile of the ducks the Ig is not IgA, but as an IgM molecule; it has
additional antigenic determinants compared to serum IgM, therefore it is probably
an independent molecule.

Secretory IgA in birds exists primarily as trimers or tetramers in place of dimers

in mammals.

The lymphatic vessels of the intestinal organs are mainly responsible for the
transport of Quilo to the yoke-subclavicular junction; these are derived both from
the endothelial cells of adjacent vessels and from mesenchymal lymphomablasts.

2.6.4. CHANGE OF ISOTIPO (MAMMALS):

It occurs mainly during immune responses

T cell-dependent; when the response is independent T the predominant isotype is
IgM.

The B lymphocytes that produce IgA or IgG have been

found in the neonatal spleen indicating that isotype change can occur without the
help of T helper cells or without antigenic stimulation (this would be an atypical
event).

The idea is that the basic change from IgM to the next Ig
in sequence (IgG3 in the mouse), etc., is programmed basic process of
differentiation and occurs during cell division, that is, T cells and antigenic
stimulation are not necessary for the change event but under normal circumstances,
strong signals They are indicating when and from which class they are chosen.

The control of T cells is mediated by cytokines; with some cytokines responsible

for the different events (i.e.IL-4 is important for switching to IgG1 and IgE, IL-5
is important for IgA and IgG2a in mice).

Mature B cells can express more than one cell surface antibody because the mRNA and
surface Ig are maintained after the isotype change.

For the development of B cells in plasma cells the presence of antigen is required;
the plasma cells
they only produce a single type of isotype.

Most isotype changes occur during the

proliferation (after finding the antigen), in addition the process is highly
repetitive and occurs depending on the stimulus (antigen or possibly others) for
the subclasses of IgG (mammals) and also for the location of the IgE and IgA
producing cells.

3. Selective induction of different types of immunity

Develop a vaccine that is capable of producing

IgG and IgM antibodies are relatively easy.

However, it is much more difficult to develop a vaccine that induces cellular

immunity or mucosal immunity.

The nature of the vaccine and the route of administration are important.
Subcutaneous or intramuscular injections of a bacterin or dead type vaccine will
stimulate the immune system to the production of IgG and IgM type antibodies.

However, there is a very low production of IgA that protects mucous surfaces and
dead products are not very effective at inducing cell-mediated immunity.

The induction of cellular immunity requires either a modified live vaccine capable
of replicating in the animal or a killed vaccine with an effective adjuvant.

Adjuvants that have traditionally been used in vaccines for use in animals, such as
aluminum hydroxide, are not very effective in inducing cell-mediated immunity.

New adjuvants that are being developed show to be very promising since they induce
immunity
cellular even using dead vaccines.

There are some dead type vaccines that have been available and effective for many
years for certain types of systemic diseases.

These are generally diseases that can be controlled by the presence of circulating
antibodies of the IgG type.

The route of administration is important when attempting to induce local immunity,

specifically in the mucosal areas.

To obtain the production of secretory IgA on mucosal surfaces, it is best for the
animal to be exposed to the vaccine directly through the mucosa.

This can be achieved by administering an oral vaccine through food or water, by

aerosol (spray), then the animal will inhale it or by the direct administration of
an oral vaccine or nasal pits, or even in the eyes.

If a spawner is exposed to a vaccine or infectious agent in the intestine, she

could respond by producing secretory IgA, not only in her own intestinal tract but
also in her oviduct; due to the process of formation of albumin in the oviduct,
there would be IgA in the albumin and consequently in the embryos; this albumin
would be ingested by the embryos, in the final stages of their embryonic
development before hatching, when they break the shell and use the allantoic fluid
as their first source of food.

This is why the secretory IgA present in albumin can protect the chicks against
infectious agents present in the intestine of the reproductive hens.

Enteric diseases developed with some microorganisms are not controlled by the
presence of IgG and IgM antibodies in the bloodstream or by cellular immunity.

If a modified live vaccine is given by injection, but reaches the mucosal surface
to replicate, it could induce a secretory IgA response.