or Malaysia-born Chinese and less than
20% of recent migrants from China are
sensitized to HDM. Monosensitization to
HDM (over 80%) is a typical phenotype in
Singapore- or Malaysia-born Chinese as
less than 30% of them also had sIgE for
other allergens and few of the HDM-sIgE-
negative individuals reacted to other
allergens. Interestingly, migrants to
Singapore, a tropical urban city,
increasingly became sensitized to HDM
and increasingly demonstrated symptoms
of AR and asthma. More than 40% of
migrants from China who resided for more
than 8 years in Singapore had positive SPT
to HDM. Westman et al. found from birth
cohort of 2413 children that isolated
parental AR increased the odds of AR.
Having all three atopic conditions (AR,
eczema, and asthma) conferred the highest
odds for offspring AR and nonallergic
rhinitis (NAR) (Ng & Wang 2015).
“Atopic march” refers to the natural
history of allergic diseases. Atopic diseases
of different organs and causal allergens
develop sequentially with age; some
symptoms become more prominent over
time, while others subside. AD generally
develops first, followed by
immunoglobulin E (IgE)-mediated food
allergy (FA), allergic asthma (AA), and
allergic rhinitis (AR), which result in
increased sensitization to food and/or
environmental allergens. AD is regarded as
the starting point of atopic march and the
risks of FA, AA, and AR increase as the
severity of AD increases (Tsuge et al. 2021).
According to Gell and Coombs, AR
belongs to type I hypersensitivity reactions
mediated by IgE, and its pathogenesis
occurs in three phases: sensitization, re-
exposure or provocation causing rapid
allergic reaction (RAFC), and late-phase
allergic reaction (RAFL) with chronic
inflammation (Casale TB et al, 2002;
Luskin AT et al, 2004).
Allergic rhinitis is the most common
form and a prototype of IgE-mediated
disease. The hallmark of allergic rhinitis is
an IgE mediated, type 1 hypersensitivity
reaction to an inciting inhaled allergen. The
result of this reaction is a cascade of
immunological and biochemical events
leading to clinical expression of the disease.
The sensitization phase begins when
antigenic allergens enter and deposit on the
nasal mucosal epithelium. The antigenic
fragments are then processed in
macrophages or dendritic cells, functioning
as Antigen Presenting Cells (APCs). The
antigen is then bound to major
histocompatibility complex (MHC) class II
and presented on the surface of macrophage
cells. APCs release interleukin-1 (IL-1), a
lymphocyte activating factor that stimulates
Th0 (T-helper 0) cells to differentiate into
Th2 cells, which then release specific
cytokines. IL-4 and IL-13 further stimulate